Science topic

Arteries - Science topic

The vessels carrying blood away from the heart.
Questions related to Arteries
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In case of blood collection from vein and by mistake the needle inserted in artery and collected the blood from artery and the patient needed the CBC. What is the effects on CBC value you suspected?
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Compared to arterial blood, there was a significant increase of erythrocyte count (2.7%) and haematocrit (3.1%) in the venous blood. The total and large leucocyte counts were significantly higher (9.2% and 12.6%, respectively) in the fingertip blood than in the venous blood.
Reference
Comparison of blood counts in venous, fingertip and arterial blood and their measurement variation
Z W Yang et al. Clin Lab Haematol. 2001 Jun.
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doi: 10.1046/j.1365-2257.2001.00388.x.. 2001 Jun;23(3):155-9.Clin Lab Haematol
Authors
Z W Yang 1 , S H Yang, L Chen, J Qu, J Zhu, Z Tang
Affiliation
  • 1 Morphometric Research Laboratory, North Sichuan Medical College, China. zwyang@nc-public.sc.cninfo.net
  • PMID: 11553055
  • DOI: 10.1046/j.1365-2257.2001.00388.x
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I work usually with idealized geometry, but this time I want to use patient specific geometry of blood arteries. Is there any way to upload/implement such type of geometry to a Matlab code?
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Thank you Mr. Daniel Galeazzi for your answer. I will try this out.
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Dear All,
i came across different papers (mostly published between 2000 and 2010, i.e. "Predicting Arterial Stiffness From the Digital Volume Pulse Waveform") in which formulas and associations were found in order to calculate an arterial stiffness index through a pletismographic assessment.
Since the methodology seems reliable and of much easier assessment compared to tonometry, does anybody know if there are commercially available devices and softwares which may acquire digital volume pulse waveforms and provided arterial stiffness indexes?
Thanks
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You are absolutery right when consider the obtaining pletismographic wave form is much easier than pulse wave contour. However these are two different proceses: pletismography describes blood flow and pulse wave contour depicts arterial wall motions. They look quite similar but are not the same. That is why we prefer pulse wave form analysis to pletismographic data.
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Please suggest the best doppler angle to study haemodynamics of umblical artery at different stages of gestation in sheep ?
Few researchers suggest
A) 0-10 degrees (Petridis et al 2017; Elmetwally and Tillmann)
whereas others suggest B) 45-60 degree
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Sir, i am also wandering same but in general angle should be less than 60 and close to 20, this is what came to know from reading some literatures.
even i wish to know wether angle is auto adjusted once set in the machine even after movement of probe.
thank you
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hellow I need a database for my project "calcification of lower limbs artery" and i don't find any dataset for this project,Can any one help me to find it or how to research or where i find it ?!
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Dear Benzaid,
if you are not getting the data set openly, kindly find the article related to this work and sent a request to the corresponding author. Mostly they wrote it like the datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.
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With the newly characterized phenomenon of load-dependent based indices of HFpEF and HFrEF, and many more, is ejection fraction (EF) the proper index to be used to characterize failing cardiac muscle?
  • As EF is strongly dependent on operating with “hypothetical” ventricular elliptical geometry i.e., assumption of a fixed relationship between chamber dimensions and volume (PMID: 6061825; ), which are e.g., very distinct in most heart failure situations (PMID: 26417058). Moreover, EF could decrease, while contractility increases because of changing afterload, represented by the effective arterial elastance (Ea) (PMID: 28953198).
  • My Q is: are there any supporting literature to Dr. Morimont's PMID: 28953198 (above) or from your own experimentation that suggests that when LV volume decreases from EDV to ESV, the actual ESV is a function of not only intrinsic heart contractility, but also of this arterial load. For the same EDV and intrinsic heart contractility, if arterial pressure at end-systole decreases (i.e., Ea decreases), then ESV is lower and LVEF greater? Thank you kindly for your answers. Filip
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The whole data set during stress Echocardiography can include the volumes of the left ventricular so that. Ejection fraction is derived from end diastolic and the end Systolic volumes. In normal person with excercise end Systolic volume decreases and hence we get increase ejection fraction. But in some normal person who gets hypertensive responses show no changes or increased end Systolic volumes and eventually decrease ejection fraction during excercise. This happens because of increase peripheral vascular resistance ehich causes decrease cardizc out put despite increase cardiac contraction.
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Blockage of arteries is a common problem during theses days, which may lead to myocardial infraction or heart attack. Once the plaque is formed, it cant be removed. The problem can be overcome either through bye-pass surgery of heart or by putting a stent at blocked portion of the arteries. So my request is to know that is there any chemical individually or in combination in Allopathy / Ayurveda that can reverse the plaque formation.
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Thanks, dear Mahesh Golla for your kind suggestion.
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Heart attack has become the common problem during these day because of our life style and dietary habits which lead to the clogging of the arteries either due to deposition of calcium or cholesterol. In this context my humble request is to know that is there any proof regarding the removal of the plaque/ reversal of plaque in the arteries by the use of apple cider vinegar.
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Apple cider vinegar will not unclog your arteries or cure atherosclerosis on its own. Making long-term lifestyle adjustments, such as stopping smoking, decreasing weight, and keeping physically active, is crucial.
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No doubt Arjuna has many medicinal properties like antioxidant, anti-inflammatory and antimicrobial, strengthens and tones the heart muscles, helps in proper functioning of the heart. Arjuna tree also has strong anti-hypertensive property and helps reduce high blood pressure. In this context my request is to know that is there any scientific study or proof regarding the removal of the plaque/ reversal of plaque in the arteries by the use of Arjuna (any form).
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Please visit the following RG link for insights.
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I need to simulate a pulsatile flow in the artery.
Does anyone know how to do this in Comsol or how to change dependent pressure in the main Navier-Stokes equation with a variable pressure with time?
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You can put function with time by inputting equation in f(x) Analytic (an1) [arguments: time]. You can also use Gaussian pulse (gp1) to make your function smoother in order to prevent convergent problem. Hope this can help!
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Which is the most adequate model to represent the physiological waveform of pulsatile blood flow in large arteries?
Many models exist in literature (Mcdonalds model, Sherwins model, ...)
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In my opinion, although not perfectly, the I profile curve corresponds to the velocity profile in the iliac artery. It is certainly the best representation of those you have presented. Remember in addition the period of the function, which is most often taken in the literature as 0.8 s, which corresponds to 72 heartbeats per minute or 1 s - 60 beats per minute.
I wish you luck in implementation,
Damian
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Hi
I am planning to reconstruct 3D geometries of coronary arteries from angiogram images (not a single artery whole coronary artery trees). I am wondering if any of you have any software suggestions that can help. Or any potential Matlab/Python codes that can help?
I know that there is some open-source software that can be used for CT or MRI images. But I couldn't find any for angiogram images.
Thanks for your help.
Navid
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Dear All,
Hope you are doing well.
How to draw a line in center of the artery fluid volume domain. The problem is that, the line/plane couldn't fall properly at center of artery. When i use the option "LINE command from Location in ANSYS Fluent post processor.
The geometry or model was extracted from patient CT scan data so which is not in a single plane.
Thanking you in anticipation.
&
Regards,
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Faheem Ejaz add line/plane?? Yes, i used same to draw above shown yellow line but my question is about exact center of fluid volume or at mid of axis i want to draw a line. I know ur options , those are also not workout.\ Thanks
Regards,
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I am doing modelling of arteries and I have completed solid mechanics part. Now I have to do FSI to obtain Pressure and Wall shear stress.
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Is there any way to couple ABAQUS and Ansys(fluent)?
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Atherosclerosis is a specific type of arteriosclerosis.
Atherosclerosis is the buildup of fats, cholesterol, and other substances in and on your artery walls. This buildup is called plaque. The plaque can cause your arteries to narrow, blocking blood flow. The plaque can also burst, leading to a blood clot.
Although atherosclerosis is often considered a heart problem, it can affect arteries anywhere in your body. Atherosclerosis can be treated. Healthy lifestyle habits can help prevent atherosclerosis.
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As we know that Fat , cholesterol and other substances like Calcium , are the building block for the formation of plaque inside the lumen of coronary arteries , partially or totally block the blood flow to heart , leads to Ishaemia or infarction. There is no specific novel biomarkers to assess the progression of atherosclerosis. Besides the usual novel biomarkers like BNP , NT-Pro BNP , tropinin HDL-c , HDL function ,now researcher are eager to find out the novel biomarkers( produced by cardiac tissues) like miRNA , protein , fat by use of new technologies like Mass spectroscopy ,pcR bases array and MS based lipidomics
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Dear Experts
I am a student of Biomedical Engineering. I am doing my thesis on effect of eccentric stenosis in coronary artery. I had a query regarding calculation plaque eccentricity index. I used calcification  tool and separated calcification from the coronary artery. But, the calcification reconstructed from MIMICS is not near the wall but near the center of the artery path (Figure-1). Shouldn't the plaque be located near the wall?
Thank you.
Regards
Noushin
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Abdul Gaphur as the image provided is 2D, I understand your concern. However, it's not attached to any surface (according to the 3d view). Thank you.
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60yr old female post cholecystectomy and post hysterectomy presented with paralytic ileus
On CECT portal vein is getting opacified in arterial phase
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Selective angio of the celiac trunk or better superselective angio of the liver artery (a. hepatica propria) to identify suspicious av fistula. Therapy (embolisation/stentgrafting) can be done I same session, but only if there is a medical indication.
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Hello! I'm trying to perform the perfect stain in portal vein. I have stained it with H&E. I have some questions:
1.- Has someone observed the histology of portal vein?
2.- Is it possible to observe atherome plaques there?
I'm used to seeing arteries and plaques inside the artery but I'm new in veins.
3.- Is there any specific stain for veins better than H&E?
Thank you!
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María Martín-Grau I hope you find these answers helpful.
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I have been always told that the venous (mixed venous of Central venous) PO2 does not go above 40, even if the arterial PO2 is elevated to very high levels (say 150) by increasing the FiO2 in cases where there is no increased tissue demand
Why would the venous PO2 not rise?
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Friends,
I have no definite answer to my own question
But I did a small trial. For my patients in ICU (most were intubated), I increased the FiO2 to 100% and did the ABG as well as a VBG (from the CVP line in the neck)
Let me give you the paired readings of 7 patients (ABG Po2/ CVP Po2)
Pao2 315/ Pvo2 63
349/<40
355/<40
287/54
407/<40
149/49
194/<40
So it looks like in some cases, the Pvo2 can go upto levels of 60
All the cases where the Pvo2 was > 40 were cases of shock (septic) on inotropes
And all the others with Pvo2< 40 were not needing inotropes
This may confirm the theory that in sepsis, the O2 uptake by tissues may be impaired (? mitochondrial dysfunction) and the hence the O2 content in the venous blood may be elevated
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I'm looking for a website which have the files of real arteries and arterial bifurcations to import to Ansys meching.
Can anyone introduce such websites?
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hi pooyan. how are you?!
i suggest to visit the grab cad website and search for Artery.
i hope you find what you are looking for.
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I'd like to ask about normal values /categories related to arterial stenosis for Common carotid artery and Posterior tibial artery duplex : Vmax, Ved, Vmin, Vm_mean, RI, PI, S/D
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For significant carotid artery Stenosis following criteria :
Peak Systolic velocity in ICA more than 215 cm /seconds
Peak diastolic velocity in ICA more than 100cm/sec
Ratio of PSV between ICA and CCA more than 4.0.
According to society of radiologist and Ultrasound concensus criteria.
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I want to know how many isolated rat pulmonary artery rings, I can get from a rat, for use in the organ bath. So how long is a rat's main pulmonery artery. Thank you.
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Unless there's a powerful reason for not using other arteries, I would use the PA (pulmonary artery) but all other big arteries as well (aorta, carotid, femoral) in the first experiment to maximize the use of one animal life. - In the same experiment I'd measure the length of the PA as well as other arteries (take a picture of the dissection). In the second experiment, you are better positioned to focus on the PA artery rings, assuming all other rings are not useful. Besides pressure, are there other variables that make the PA unique for your investigation?
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I am studying the blood flow in arteries and want to do certain simulations in coronary, carotid, and femoral arteries. But I did not find any paper where the values of Reynolds number are given for the blood flow in these arteries. I will be grateful if you share the details of the reference paper/book/article which I can use to cite the values of Reynolds number.
I have taken Re=600 to simulate blood flow in a coronary artery. Please help me regarding this.
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"...The typical Reynolds number range of blood flow in the body varies from 1 in small arterioles to approximately 4000 in the largest artery, the aorta..." Ku DN. BLOOD FLOW IN ARTERIES. Annu. Rev. Fluid Mech. 1997. 29:399–434
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Sphygmocor is the tonometry based instrument which is used to record generally radial pulse waves and then calculating various variables like Augmentation Index, SEVR etc. It is also used to calculate pulse wave velocity. I have downloaded 2-3 papers on same research which have calculated pulse wave velocity in their studies and ultimately got information of arterial stiffness in those studies. however calculating pulse wave velocity by methods elaborated in these studies is cumbersome as it requires recording pulse of poplitial artery whose recording is again a cumbersome process. Can anyone suggest easy method to calculate pulse wave velocity using this instrument so that i can comment on arterial stiffness in study population.
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Clasical pulse wave velocity (PWV) estimation in the elastic arteries is a measuring of the wave propagation alongside of aorta: from carotid to femoral artery. When you evaluate PWV in muscular-type arteries you use a sector from the carotid to the radial artery. In Sphygmocor device the software evaluates the delay of the pulse wave onset in each site of investigation (carotid, femoral and radial artery) to R wave on ECG. If the heart rate is the same (constant) the software calculates PWV. The main problem of this device is the requirement of constant heart rate. In other type of devices (Complior, etc.) you can record pulse wave from two or three sites simultaneously and it could be more accurate PWV estimation in comparison with Sphygmocor. However, all these devices are recommended for PWV evaluation.
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During initial stages of transradial arterial route for interventions : which is better single wall or double wall puncture
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Thank you for sharing this Question
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Performing pulsed Doppler ultrasound on a single thyroid artery (upper or lower; right or left) is it sufficient for the study of the mean sytolic peak in order to differentiate Graves' disease and Hashimoto's thyroiditis thyrotoxicosis.
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NO!!!! Systolic pulse can be altered in many situation, not only in hyperthyroidism. Hashimoto's thyroiditis is most frequently associated with hypothyroidism, but we must not forget that "hashitoxicosis" does occur too.
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Hi ORO experts,
I'm struggling with ORO background precipitates in arterial tissues. The protocol I use works very well on human atherosclerotic plaques which are full of lipids and I don't notice the background, but when it's a healthy artery with only droplets of lipids I see lots of precipitates from ORO solution. I use ready to to use 0.5% ORO/isopropanol solution from Sigma which I dilute in water (60%), leave for 10min and filter (tried all sort of filters: 0.22um, o.45um, whateman paper and a combination of whateman paper/0.22um filter). Tissues are then immersed in 10% neutral buffered formalin for 5 min, then 5 min in 60% isopropanol, ORO was added to all tissues (positive control is the human plaque) and incubated for 10min. Slides are then immersed quickly in 60% isopropanol then wash in water before I counter stain with haematoxylin. everything works except the precipitates. I tried warming but the same issueup the solution in a heat block @ 60C for 2 hours as well . Any idea how to fix this please? thanks in advance!
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Thanks
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For example, how can it differ from ordinary derivative or calculus. Actually, what kind of results or outcomes can be obtained by using fractional derivatives.
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see the following paper
A Study of Fractional Relaxation Time Derivative on Blood Flow in Arteries with Magnetic and Thermal Radiation Effects
Abstract:
In this paper, a fractional relaxation model is studied to determine the effect of heat transfer and magnetic field on the blood flow. The flow is due to an oscillating periodic pressure gradient and body acceleration. We apply Laplace transform as well as finite Hankel transform to obtain the closed-form solutions of the velocity and temperature distributions of the fractional time partial differential equations. The effect of the fluid flow parameters is shown graphically with changes in the ordinary model as well as the fractional parameters. The analysis shows that a fractional derivative is an excellent tool that gives a remarkable change in controlling temperature and blood flow. The analysis depicts graphically, that the presence of a strong applied (exterior) magnetic field, reduces the temperature and blood flow velocities, which is appropriate to avoid tissue damage during treatment. Besides, it is seen that some of the aforementioned parameters influenced the fluid flow profiles in an increasing and decreasing fashion which is interpreted as useful to the study.
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The arterial blood gas analysis (PaO2, PaCO2, pH, HCO3p, BE(Ecf),....) are changed during cardiopulmonary bypass depends on patient condition and perfusion management. is there any reference values upon which we can say that the patient has metabolic/respiratory acidosis or alkalosis?
Thank you in advance
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Determining acid-base status of a patient under cardiopulmonary bypass
Have a look at these informative articles:
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I collected data for independent different physical examination skills (Blood pressure measurement, Auscultation of heart sounds , Auscultation of lung sounds, heart rhythm assessment, and palpation of arterial pules).
the data collected to see how relevant was the simulation experience with mannequins for those physical examinations.
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the examinations are according on the type of analysis.
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I calculated the flow in arteries and I would like to show that for some time steps the wall shear stress has the opposite direction, for example in the curves, branches, etc. For the straight pipes it is easy but how to do it for the more complicated geometries?
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First enable boundary flux in physics settings~ then u can use the expression like stress dot product with boundary coordinate system (like nx t1x and t2x etc) manually putting in the variables to find the components of interface tractions (normal shear1 and shear2).
You can also plot in 5.5 to see the directions of each traction.
Also check the supplementary information of my paper (debonding mechanism in electrochemical society) I have calculated the normal and shear tractions and showed how their direction changes with respect to the charging time...
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Does any one know what is the theoretical point of weakness in the lateral skull and what bones is it formed of?
And If someone was diagnosed with an intra-cranial haemorrhage
what is the most likely blood vessel from which the haemorrhage is originating and through which opening does this artery enter the skull base?
Also what would be the most common type of haemorrhage and what is the anatomical basis for this.
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-Pterion is an important landmark for the anterior branch of the middle meningeal artery, which underlines this area on the inside of the skull. It is not a single point but an area where the frontal, parietal, squamous part of the temporal and greater wing of the sphenoid bone adjoin one another.
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In my lab we work with multiple vascular beds using pressure myography to test endothelial dependent vasodilation (i.e. acetylcholine and/or insulin). It is of our interest to detect NO levels after stimulation using confocal microscopes and we have used protocols used in papers and also made changes from answers to questions here in RG. So far we have not been successful, I would really appreciate if someone could give me an advice or a protocol that works.
In short what I want to do is:
1. After temperature equilibration, pressurized arteries under static conditions at 37°C will be challenged with 80mM KCl to test vessel viability.
2. Arteries are washed 3x with PSS and wait for 5 mins.
3. Myograph chamber is translated to confocal microscope with temperature controlled system set at 37°C and we wait for 1 mins to the vessels to adjust to the new environment.
Here is my questions:
Some protocols say:
Incubate in acetylcholine (for exmaple) for 10 mins and after that incubate with DAF-2DA (5µM) for 30 mins and both steps at 37°C. Wash 3x for 1 min and fix with 4% paraformaldehyde and then add DAPI and image. You will only have a time measurement of NO.
A different protocol says to incubate with DAF-2DA (5µM) first and then take an image at t=0, add acetylcholine and incubate for 10 mins and take an image every 30 mins after that.
Those protocols are either for cells or aortic rings using en face mounting to image. What I want is a pressurized vessel, so I think the best option is to add DAF-2DA intraluminally and add acetylcholine to the vascular bath. But what option is the best, Should I incubate with acetylcholine first, or with DAF-2DA first? Should I fix my artery before imaging or should I do a time-dependent experiment? Is there any normalization taht I should use to help with the analysis? Is there anything else I should pay attention?
Thank you for you time in advance.
Francisco I. Ramirez-Perez
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Hello Francisco,
If you are planning on monitoring NO generation real-time, then any grossly invasive procedures seem not very productive for your goals.
Given that NO is actually a diffusive gas, prolonged and elaborate procedures prior to detection add to possibilities of artificial outcomes. Therefore, the additional staining like DAPI is actually not advised, if NO staining itself is already challenging enough. It also concerns the magnification of info at which you want to show -- NO as detected by DAF-FM, for example, is best presented at the whole cell or cell population level (tissue sections), not at the subcellular level (thus, counter-staining with a nuclear DNA dye does not help much).
Probe incubation followed by prolonged PFA fixation and detection is not ideal, because these procedures tend disrupt cell membranes and alter permeability signficantly. DAF series probes are small molecules, and fixing will reduce the chance of their fluorescent products being detected (false negatives).
Please consult our paper on staining mouse vessels with a fluorescent probe for peroxynitrite (ONOO-), an RNS derived from NO, using a protocol involving live tissue probe staining by perfusion, brief PFA fixing, embedding, cryosectioning, and finally confocal imaging. (See details in SI). This method should work for other small-molecule fluorescent probes provided they are sufficiently retained and survive the fixation and wash steps performed by the experimenters.
In general, if you are interested in test acute drug effects, the procedure would be:
- pre-loading the NO probe (to a final recommended conc.) into the cells or isolated/bathed tissue. Typically 30 min will do. Wash is usually not needed at this stage unless the commercial protocols state so, or you can test it out in imaging, to see how much fluorescence survive following washes.
- add the drug to simulate NO production. Allow sufficient time for build-up.
- terminate the incubation by a lavish wash (2x original volume for example) or directly proceeding to PFA fixation (5 min, on ice; 4% PFA in PBS).
- Wash lavish 1-2 times to remove residual PFA (when dried, or concentrated, this becomes autofluorescence or other artifacts).
- proceed to OCT embedding and normal cryostat sectioning (low temp.). Do not use paraffin embedding, which will invariably fail.
- mount sections onto a glass slide with coverslip (plus anti-fade Gold, Invitrogen), for imaging (confocal, magnification at 40x or 63x).
Good luck.
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Positioning the bedridden patient in prone lying at frequent intervals in 24 hours can be helpful in avoiding so many complications of chest as it directly effects on improving perfusion and arterial oxygen level.But unfortunately due to lack of awareness adapting this position mostly gets neglected.
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Who will bell the cat for bed-ridden COVID-19 patients?
Bedridden COVID-19 patients, whether children, adolescents, or adults need to be helped to prone position by a care-giver at home or by a nurse in the hospital.
One has to make sure that the positions are changed to avoid causing another evil while managing COVID-19, the pressure sores.
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Hi, Has anyone used 2F Fogarty Arterial Catheter from Edwards lifescience recently? I had used this product for rat carotid artery injury for more than 15 years and never had problems until recently. The balloon catheters I ordered (totally 3) had such thick bulge connection between the balloon and catheter and it is impossible to insert the catheter into rat carotid arteries (even with 500g rats) without tearing the artery. I left a message to the salesperson and it has been over three months, no response at all. I was wondering if there is any other suppliers exist. We are in the middle of the project and devastated to find a new supplier.
Thank you,
YC
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Try LeMaitre Vascular: good quality.
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Dear community,
I am looking for whole-body MR angiography images. I would be very grateful if someone could recommend me any resource, or would like to establish a data sharing agreement.
I am currently designing a numerical model of the cardiovascular system. In this context, I need to know the position and orientation of the main arteries of the human body in several healthy specimens. If you have other solutions than whole-body angiography to get these parameters, then I would be also very happy to read your recommendations!
Thank you in advance for your help!
Best regards,
Jérémy
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I’m not familiar with the whole body MRA, as far as I know it’s been using in PAD patients. But it sounds like taking forever!
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On table 3 from paper was mentioned some characteristics that we would like to complete with more information that allow us associate arterial events with another risk factors, adherence to rivaraxoban or % of autoinmune diseases for example.
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In other word there was no predictor for arterial thrmbosis
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We have tried calculating the artery to venal ratio,but on calculation the ratio is remaining unchanged for different images.we are unable to debug it.
# detecting artery and vein
mask2 = cv2.imread('D:/Desktop/MINI PROJECT/Hypertensive-Retinopathy-Detection-master/image01.tiff')
imgseg = cv2.imread('D:/Desktop/MINI PROJECT/Hypertensive-Retinopathy-Detection-master/inverted01.tiff')
_,mask2,_= cv2.split(mask2)
cv2.imshow('segmented image',mask2)
print(mask.shape,mask2.shape)
count = 0
intensity = 0
for x in range(mask.shape[0]):
for y in range(mask.shape[1]):
if mask[x][y] and mask2[x][y]:
intensity = intensity + imgseg[x][y][1]
count = count + 1
print('intensity sum {}'.format(intensity))
intensitymean = int(intensity/count)
print('intensity mean {} and count {}'.format(intensitymean,count))
artery = mask.copy()
vein = mask.copy()
cv2.imshow('artery before',artery)
cv2.imshow('veins before',vein)
for x in range(mask.shape[0]):
for y in range(mask.shape[1]):
if mask[x][y] and mask2[x][y]:
if imgseg[x][y][1] >= intensitymean-15:
artery[x][y] = 0
else:
vein[x][y] = 0
cv2.imshow('artery',artery)
cv2.imshow('veins',vein)
cv2.imshow('whats this',vein-artery)
# arteriovenus ratio
# invert
artery = 255 - artery
vein = 255 - vein
cv2.imshow('inverted artery', artery)
cv2.imshow('inverted vein', vein)
#cv2.imwrite('F:/DESKTOP/Downloads/Hypertensive-Retinopathy-Detection-master/artery.tiff',artery)
#cv2.imwrite('F:/DESKTOP/Downloads/Hypertensive-Retinopathy-Detection-master/vein.tiff',vein)
# distance transform
print(artery.dtype)
arteryDist = cv2.distanceTransform(artery,cv2.DIST_L1, cv2.DIST_MASK_PRECISE)
veinDist = cv2.distanceTransform(vein,cv2.DIST_L1, cv2.DIST_MASK_PRECISE)
cv2.imshow('distance transformed artery', arteryDist)
cv2.imshow('distance transformed vein', veinDist)
#cv2.imwrite('F:/DESKTOP/Downloads/Hypertensive-Retinopathy-Detection-master/veinDist.png', veinDist)
# thinning
kernel = cv2.getStructuringElement(cv2.MORPH_CROSS,(3,3))
size = np.size(arteryDist)
arteryskel = np.zeros(arteryDist.shape,np.uint8)
done = False
while( not done):
eroded = cv2.erode(arteryDist,kernel)
temp = cv2.dilate(eroded,kernel)
temp = cv2.subtract(arteryDist,temp)
arteryskel = temp.copy()
arteryDist = eroded.copy()
if cv2.countNonZero(arteryDist) == 0:
done = True
print(cv2.countNonZero(arteryskel))
cv2.imshow('thinned image artery',arteryskel)
veinskel = np.zeros(veinDist.shape,np.uint8)
done = False
while( not done):
eroded = cv2.erode(veinDist,kernel)
temp = cv2.dilate(eroded,kernel)
temp = cv2.subtract(veinDist,temp)
veinskel = temp.copy()
veinDist = eroded.copy()
if cv2.countNonZero(arteryDist) == 0:
done = True
print(cv2.countNonZero(veinskel))
cv2.imshow('thinned image vein',veinskel)
venuole = []
arteriole = []
for x in range(veinskel.shape[0]):
for y in range(veinskel.shape[1]):
if veinskel[x][y] > 0:
venuole.append(veinskel[x][y])
if arteryskel[x][y] > 0:
arteriole.append(arteryskel[x][y])
venuole = sorted(venuole)
arteriole = sorted(arteriole)
lenven = len(venuole)
print('length of lenven {} {} {}'.format(lenven,lenven//2,lenven//2-1))
lenart = len(arteriole)
print('length of lenart {} {} {}'.format(lenart,lenart//2,lenart//2-1))
if lenven%2 == 1:
Wa = venuole[lenven//2]
if lenven//2 == 0:
Wb = venuole[0]
else:
Wb = venuole[lenven//2 - 1]
else:
Wa = (venuole[lenven//2 - 1] + venuole[lenven//2])// 2
Wb = venuole[lenven//2 - 1]
print("Wa,Wb",Wa,Wb)
CRVE = sqrt(0.72*(Wa**2) + 0.91*(Wb**2) + 450.02)
if lenart%2 == 1:
Wa = arteriole[lenart//2]
if lenart//2 == 0:
Wb = arteriole[0]
else:
Wb = arteriole[lenart//2 - 1]
else:
Wa = (arteriole[lenart//2 - 1] + arteriole[lenart//2])// 2
Wb = arteriole[lenart//2 - 1]
print(arteriole)
print("wa,wb",Wa,Wb)
CRAE = sqrt(0.87*(Wa**2) + 1.01*(Wb**2) - 0.22*(Wa*Wb) - 0.73)
artervenratio = CRAE/CRVE
print('arteriovenous ratio {}'.format(artervenratio))
cv2.waitKey(0)
We are not getting correct value of wa and wb hence the calculation of AVR is also coming wrong.
Could you please help us debug the code.
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Put comments in your code! Doings so will help you finding the bug(s).
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Hello everyone,
I have some questions about the stenosis in arteries and veins.
What is the limit pressure that forced the artery to be closed causing sever stenosis?
&
What is the limit that the stenosis start to be formed?
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The pressure applied on an artery to close (rather than get stenosis) depends on which artery is concerned because there are medium sized artery that have a muscular wall eg radial artery and large elastic arteries (eg aorta) and on the pressure inside the said artery. On another note stenosis is most commonly caused by disease inside the artery disease such as atheroma. I hope this is helpful
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Although complications of central venous cathter insertion have deceased with the use of ultrasound but still exist. What is the current reported complication rate ?
Thank you!!
SS
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"It takes a lot of malpractice to hit an artery instead of a vein identified by ultrasound Doppler. I believe this probability is close to zero"
Carlos don't be so sure. As a vascular surgeon I have put sutures many times on ruptured subclavian, femoral, iliac ..... (you name it) arteries after central venous line misplacement. :-D. Now seriuosly - the complication rate is estimated on 1% total, with US guidance it is said to be lower however there is no strong evidence (besides logical). … Read more
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Hi everybody,
I want to simulate a bubble moving in fluid, say blood using comsol. For such type of interfaces, to couple mesh motion with fluid motion, dose the following kinematic boundary condition is okay?.
u.n= u*nx+v*ny
or n*(u-xt).
here t is time. which one is correct?. Thanks in advance.
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I think the following links can help you. In the first case, ignore the electric field.
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Hi everyone!
I'm a graduate student and studying about bio-electrical circuits.
I want to put a circuit as close to Substantia Nigra as possible through artery, but I don't know.
I looked into Willis circle, but I don't know which is what I'm looking for.
Anyone who's familiar with this subject, please help me.
Thank you for reading!
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Posterior cerebral
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In some article, it is mentioned that arteries with diffuse atherosclerosis is easily regarded as ''normal'' arteries and are underestimated its severeness, compared to focal stenosis. I wonder why it would happen because plaques can also be observed in CTA graph.
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Coronary angiography is a luminogram and that explains low sensitivity for diffuse disease
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We are doing heat and mass transfer analysis when blood flows through a porous artery. We apply ANSYS CFX for the simulation analysis. We want to fix interfacial area density between two phases (Fluid phase and solid phase).
Any article or data or any equation that is available?
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Tytus Tulwin thank you..
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I have lung images in which I have used QuPath software to quantify total alveolar space damage. I am attempting to validate the method via linear mean intercept (LMI) measurements, however I am having trouble with the LMI method.
From what I understand I need to use ImageJ to lay a grid over my images and measure the number of intersections the tissue has with the grid (analyze particles), however I am unsure how to properly exclude any regions where there are arteries and airways which would not be considered alveolar space. Is it possible for me to draw a polygon around these regions and exclude them from the quantification? Any help is greatly appreciated!
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Unfamiliar with application here, but if you want to exclude regions from particle analysis, apply a mask. Duplicate image, add 1 to every pixel, draw a region, clear it out, turn into binary, and apply as mask (there's a plugin, or just multiply images) before doing particle analysis
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I want to develop a material for a cardiovascular stent application. Therefore, I want to know about the pressure which a stent will bear in the artery.
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The pressure at which stent is deployed has nothing to do with blood pressure. The nominal pressure for most of the stents as has been pointed out is 8 to 12 bar. But most stents require post dilatation with non compliant balloon at 18 to 20 bar. Some lesions rarely require post dilatation at even higher pressures . If the lesion and vascular bed are properly prepared, very high pressure post dilatation can be avoided, as it carries risk of vascular rupture.
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I want to simulate blood flow in stenosed artery using OpenFOAM.
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You can start with wolf dynamics website. I learned with it and its free of cost. For more help take printout of manual.
Don't hesitate to perform wrong simulations. It will add up to your accuracy.
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Very important findings by memory disorders, demnetias and schizophrenias!
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The artery models are not patient specific CT models, rather, CAD models based on previous knowledge of human body.
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Blood flow is an non-Newtonian fluid so you can use a fluid that near to blood properties and make numerical simulation representing the actual case study.So the mechanism including the non-Newtonian fluid case can be used in validating the actual case study.
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What medium/solutionand techniques would you recommend for the storage/freezing of human artery tissue biopsies for further DNA isolation?
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Wow!
I don't think that any of the above answer would be nesecary.
Just freeze your biopsies in -20 or -70.
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Now,I want to extract RNA from artery wall in mouse,but there are lots of fibrosis in artery wall.I can't get sufficient RNA concentration(only 15ng/ul).and my tissue section is very small(only 1mm*1mm).Please help me!
my kit is direct-zol RNA MiniPrep
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Try crushing the tissue into powder before adding TRIzol reagent. Arterial tissue should be easily crushed when it is frozen in liquid nitrogen.
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Pro:
1. Significant elevation of splenic artery blood flow ( +1 l average -our data)
2. Proved effect of NSBB
3. Proved effect of diuretics
4. Good clinical effect after splenic artery embolization (our results)
5. Proved hyperdynamic circulation in portal hypertension patients
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Dear Dr. Kozlov:
I get the PDF file of Chapter 92, Portal Hypertension and Esophageal Bleeding,10th edition of Sleisenger and Fordtran's Textbook of Gastroneterology and read the hemodyanamic principle of portal hypertension. The pathophisiology of splanchnic hyperdynamics is still the same as what I have understood.
An mechanism of A-V shunting may exists between the splanchnic, intrahepatic or pulmonary vessels. Splenic A-V shunting is the most common type of splanchnic hyperdynamic state and your result can support this theory, better than my case report.
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The objective of the position is to develop a PhD work on the subject “cardiovascular stent design and analysis”. The aim of the work will be to analyze the expansion of the stent and the contact with the artery to simulate thrombectomy technique. The developments will have to be carried out within the Kratos framework.
More info:
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Is this position still vacant? Please let me know email ekram.aust08@gmail.com....thanks in advance
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We have been doing dissections of small arteries and collateral arteries in rat. We have been dissecting out and splaying open the femoral artery and one of its major branches (we usually refer to it as the profunda, as that is the human analog). The blades of the spring scissors we use are just a little too broad to fit effectively - it sort of works, but stretches the vessel a little to make a cut. Any suggestions? I have been looking at these as possible replacements:
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Hi Dylan,
In our lab we dissect mesenteric arteries and coronary atteries with relative ease, using scissors with the same specifications as product FST Item # 15000-03. Best of luck!
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I am working on blood flow simulation through arteries and want to know the effect of artery wall(deformable) properties on fluid. I am not getting how can I see the effect of structure on fluid.
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Try to solve the problem by using "System Coupling". I think this video tutorial can be helpful.
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I am doing my research on blood flow simulation through arteries. artery walls are considered as deformable. I want to know the effect of change in properties of artery wall on fluid by using fluid structure interaction. should i go for transient - structural ??
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From my simplistic point of view:
Considering the vascular system as a system of significantly elastic tubes, I would expect something like a propagation wave or a delay somehow proportional to the heart distance, vein/artery caliber.
Any tip?
Thanks!
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Hi Sergio,
Thank you! I understood that the fluctuations in the brain and scalp are synchronised and your tip simplifies the things a bit for me, but I am more interested in the relation (of these fluctuations) to the heart cycle. I need to read the paper you suggest now.
Thanks.
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Attached is the ECG tracing obtained from a rat on which coronary artery ligation surgery was performed. How to identify which wave is what?
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thanks a lot Mr Emiliano Diez .I need a protocol to obtain rat ECG using an ExAO.CAN YOU HELP ME?
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My goal is to insert catheter full of saline in femoral vein of rats and then I can intravenously inject pentobarbital through linking catheter to a pump. However, I face a problem. When I succeed to insert it, I always find that there is some saline leaking. I guess that I must break the vein when I insert it. But there is no blood when I separate the vein and the artery. Sometimes it is fine at first, and then the vein starts leaking out saline so I fail to link the catheter to the pump.
Does anyone face the same problem like I do?
How to solve it?
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Keep a surgical thread tight knot on femoral vein which was inserted with catheter.
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I want to modal 2d blood flow using fluid structure interaction in case of a blocked artery, I've a geometry ready, but I'm unable to model it as I'm new to the software
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Use COMSOL, add FSI (fluid structure physics) additional add non-Newtonian viscosity model for blood. Read literature.
Best of luck.
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We're looking to label the arteries and veins separately within mouse brain tissue but are unsure how to do that. Does anyone have knowledge about how to go about doing this, such as which antibodies to use? I'm relatively new to immunohistochemistry and would appreciate all the help I can get.
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Thank you Robert once again. I'll look into trying this method. @
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Hi all,
I've been starting using Amira for image analysis and I am having issues on aligning and subsequently merging 5 stacks. I need to have these 5 stacks completely aligned (these are from the optic nerve head and in the middle there are the artery and the vein which I see they are completely misaligned among all stacks). Once these 5 stacks are aligned, I need to merge them and reconstruct the 3D of the optic nerve head.
How can I align the 5 stacks? I tried to merge the original stacks together and then align them afterwards but I ended up with a mess. And if I align them separately when I merge them, the artery and the vein are still misaligned.
I really don't know how to overcome this problem, I tried several time.
I also tried to concatenate them in image j first, then import the whole stack (a merge of 5 substacks together) and then align them.
But nothing good came out.
Please, does anyone have suggestion?
Thank you
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Firstly, you have to number your sections. Secondly, sections are imported into Amira which followed by voxel determination. Thirdly, you can choose the align module in Amira. Subsequently, the file is in .am format. Lastly, you label the areas of interest individually. This is briefly explaination. The better way is the tutorial in Amira.
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I ask because the Waldorf School of Tucson exists only for the business and other well-off people. It brings up children in separateness and doesn't engage in challenging stereotypes of different classes of people that the students will meet through life. While these children may relate to people of color, these will be people of color who are children of doctors and factory owners. Can't we ever address these internal contradictions that leading to educational "hardening of the communicative arteries?"
Ich frage, weil die Waldorfschule von Tucson nur für das Geschäft und andere wohlhabende Leute existiert. Es bringt Kinder in Abgehobenheit hervor und beschäftigt sich nicht mit Stereotypen verschiedener Klassen von Menschen, die die Schüler durch das Leben treffen werden. Während diese Kinder mit farbigen Menschen in Verbindung stehen können, sind dies farbige Menschen, die Kinder von Ärzten und Fabrikbesitzern sind. Können wir diese inneren Widersprüche, die zu erzieherischen "Verhärtungen der kommunikativen Arterien" führen, nicht immer angehen?
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Dear Gloria, dear Colleague Anton Elkin, thank you very much for this discussion. Many and complex questions have been touched on here which have occupied me for a long time.
I will start my own research project on the German reform teacher Peter Petersen, who became a teacher at a grammar school in Hamburg shortly before the First World War after his broad university studies. He already played a leading role in the reform movement of education in Germany at that time, and in the Weimar Republic he formed his own state-approved reform school. His pedagogy was named Jena Plan - not by himself, but by the organizing committee of the New Education Fellowship - an international reform association - because Petersen was professor of pedagogy at the University of Jena (Thuringia) since 1923. Petersen was interested to reform the public-stately school.
The Weimar Republic (1919-1933) brought also a new situation of public education. In the German Empire until 1910 existed two separate systems of education: For the lower classes the elementary school, 8 years, also the teachers had only this elementary education.
The middle- and upper-class children attended 3 years private preschool and with the age of 10 the changed to grammar school which gave the graduation for universitry. The fee for higher education was also a reason that lower classes couldn't get a higher education; but they learned much practical things. The elementary education in Prussia took care that illiterism didn't exist, and American reformers of 19. chentury like Colonel Parker or Horace Man got some impressions for their own reform work in the States.
Elementary education was free from any fee. School education was not compulsary in the Empire-era, childern of wealthy families had a private teacher.
This two-class-system of education was broken by the Weimar Constituion. The state became responsible for all public education, private home education was not allowed, and prived school education was possible by a certain control of the state, which took most of the costs for the teachers. All children had to attend the first four years in the primary school (a comprehensive school of 4 years), then the seperate systems of higher and normal education ("Volksschule" with following 2 years vocational training) ) for the mass of children. But now the state improved the chances for the lower classes to get higher education strongly. Gifted children from lower classes could much more get higher education, although there was some school fee to pay.
Now, Gloria, comes the first question we may : Who should be responsible for education: The parents or the state? In Germany it was up today not possible to erect a general system of comprehensive school. This was the aim of the Social Democrats. We have today a situation of competition between traditional grammar school and comprehensive schools which were under government of Social Democrats and the Green Party also in fulfilling desires of parents, but - for instance - not in Bavaria. There is the CSU-party leading, we have in Germany 16 different systems of education, this considers regional traditions but is a hindrance for a uniform system. If the state weak is the private market of education strong. Many parents are not content with the public system, some "Volksschulen" or the primary school have 60 % and more children from refugees there is much trouble, conflicts and aggression - so "Waldorfschulen" (and other private schools grow), although they have to pay fee. Teacher of Steiner-Schools were not so good payed and have more to work than stately teacher. Many Waldorf-Schools need urgently teachers. A very complex situation. Also in ´East Germany Steiner School flourishes, and also in Norway and other countries, although the parents mostly are not interested in the "Weltanschauung" of Steiner. Thiere would be much to tell but I finish, now, we may continue if neeed.
Kind regards, Hein
PS. Rudolf Steiner (1856-1925) was from Austria and had studied and joined the International Theosophical Society, split off from it in 1913 and founded his own ideological society with some followers, which represented his teaching, "Anthroposophy". In 1919 he founded a school of a special kind, it was a school of the employees of the Waldorf-Astoria Group, which had its German centre in Stuttgart. Steiner, who was originally a Catholic, had his own mystical idea influenced by Indian ideas of reincarnation, which is the basis of his pedagogy. He had opted for the private school, against the state schools.
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Should fetal middle cerebral artery blood flow be assessed if the umbilical artery S/D is normal in FGR fetus? Is the same for early onset FGR or late onset FGR?
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Thank Doctor Artem Romanovsky for your answer. But in Longitudinal changes in uterine umbilical and fetal cerebral Doppler indices
in late-onset small-for-gestational age Oros D showed that the degree of placental disease in late-onset FGR cases is mild, thus UA Doppler is normal in virtually all cases, despite normal UA PI Doppler, there is a high association with abnormal CPR values. So I think MCA should be assessed both in late-onset FGR with abnormal umbilical artery and in late-onset FGR with normal umbilical artery.
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I tried the above mentioned markers and didn't specifically stain arteries alone as also veins has been taking some how a degree of staining ..any suggestions please ?
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I think you can try Elastic Van Gieson stain. It stains elastic tissue black and highlights the internal elastic lamina of arteries and arterioles. Connective tissue stains red.
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Exists a bioimpedance model/software of whole human body current and voltage distribution simulation for 4-electrode measurement (similar to DOI10.5617/jeb.173)? Preferable for matlab use where one can simulate different electrode configuration. Interesting beside would be changeable impedance for arterial and venous blood separately.
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Hi Mike,
You will probably have to create the model yourself to suit your needs, for example, from MRI dicom images. Regardless of the software you decide to use to perform the simulations, simulating a realistic model is especially challenging because it requires accurate values for the permittivity property of different tissues and fluids in the model. As of today, there are still major gaps of knowledge on the frequency-dependence of this property. Also, depending on the model complexity, another major challenge is to perform an accurate validation of the simulation setting and results.
Regards
Benjamin
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I read many articles but I could not get the proper value.
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Maybe the following papers will help you:
1. Wang Y, Cong Y, Li J, Li X, Li B, Qi S. Comparison of Invasive Blood Pressure Measurements from the Caudal Ventral Artery and the Femoral Artery in Male Adult SD and Wistar Rats. Yue J, ed. PLoS ONE. 2013;8(4):e60625. doi:10.1371/journal.pone.0060625.
2. M. JANE BLACK, TODD A. BRISCOE, MARIOS CONSTANTINOU, MICHELLE M. KETT, and JOHN F. BERTRAM .Is there an association between level of adult blood pressure and nephron number or renal filtration surface area? Kidney International, Vol. 65 (2004), pp. 582–588
3. Marina Komolova, Peter Friberg, Michael A. Adams .Altered Vascular Resistance Properties and Acute Pressure-Natriuresis Mechanism in Neonatal and Weaning Spontaneously Hypertensive Rats . Hypertension. 2012;59:979-984
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Need it for simulation purposes.
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Dear Priyam Ambastha,
You will find information in:
Wang, J. J., & Parker, K. H. (2004). Wave propagation in a model of the arterial circulation. Journal of biomechanics, 37(4), 457-470.
Willemet, M., & Alastruey, J. (2015). Arterial pressure and flow wave analysis using time-domain 1-D hemodynamics. Annals of biomedical engineering, 43(1), 190-206. link to open soruce paper: https://link.springer.com/article/10.1007%2Fs10439-014-1087-4
Best regards,
Damian Obidowski
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Hi,
Can someone suggest me is it possible to use Hemocoagulase injection for rats during surgery.
I am performing Aortic Artery constriction in rats, and I sometimes notice lot of bleeding.So, will it be worthy to use it, and also please suggest me the dose and route of administration for the same.
Thanks in advance
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I need to know how to set zero pressure before inserting the catheter to the carotid artery, So that I could get the accurate BP changes from artery.
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Please Check
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I'm doing my research work in coronary angiogram to detect stenosis using bifurcation angle measurement. till now i have done with segmenting left main coronary artery and bifurcation point detection. but I struggle finding bifurcation angle in it. please guide me how to proceed with it. I have attached image for your reference.
original image(17f32.bmp) & bifurcation point detection image(bifptimg.bmp)
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I see three bifurcations :-) !
Your skeleton is nicely 8 connected. A bifurcation pixel then has 3 neighbours in a 3x3 neighbourhood. I would take eight pixels or so (depending on the resolution) of each of the three branches, and fit a straight line to each of the three. Then calculate intersection angles of the three straight lines.
Much easier than a Hough transform, and pretty fast too!
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3-D printers are one of the almost new technologies.
Can these printers be used in biomedical engineering?
(For example, to build artificial veins and arteries, joints, and so on.)
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Applications of AM and 3D bioprinting in the field of pediatrics are diversified. The three main application categories are: (i) Surgical planning, (ii) Prostheses, (iii) Tissue constructs, and (iv) Drug printing
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The goal is to create a flow device for simulating blood flow over endothelial cells in arteries. Bifurcation angles are varying, and the branches may not have the same diameter as the main channel. I do not have access to sophisticated casting/moulding equipment.
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Hi Priyam,
Considering your channel dimensions (which is relatively large) you can use either laser micromachining or CNC to fabricate your master mold on PMMA. Then you can simply cast PDMS on it form your channel.
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I am planning a Verhoeff van Gieson stain on arterial sections: do they need to be paraffin-embedded or will the stain still work well on frozen sections? I found this protocol http://www.ihcworld.com/_protocols/special_stains/vvg.htm
and it has a brief line: "...may be used for frozen sections as well. " However, it, and most other protocols I have found, seem to suggest paraffin embedding. Has anyone used this stain with frozen sections? Does it work just as well, or are there issues?
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Dear Dylan McCreary see the following file
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Isolated Systolic Hypertension in elders is most likely due to rigidity in arterial walls . What is the reason that rigidity doesn't affect Diastolic Hypertension ?
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