Vascular Medicine

Vascular Medicine

  • Olli Leppänen added an answer:
    Angioplasty alone or angioplasty with stenting for renal artery stenosis associated with hypertension in a young girl with Takayasu arteritis?

    This 18 year old girl was detected to have Takayasu arteritis with hypertension during evaluation for polyarthralgias. MR angiography revealed her to have severe renal artery stenosis left and left subclavian artery stenosis. Recent literature seems to suggest a higher failure rate and restenosis with stenting rather than with plain angioplasty. This goes contrary to what we see in atherosclerotic coronary artery disease stents have a higher success rates. 

    Olli Leppänen

    Dear Dr. Subramanian,

    There was a pretty good contribution from all of the people in this Q&A thread. I am happy that the patient is doing well.

    all the best for you as well as the other colleagues in this thread.

    best regards


  • Piotr Kabata added an answer:
    What other symptoms or signs would be associated with clubbing in patient of cannabis abuse?

    I have a patient who has gross clubbing of fingers and toes, who is smoking cannabis for last 15 years, 10 cigarettes a day. He is underweight with BMI of 22.5. I also noted epigastric mid line hernia.

    • [Show abstract] [Hide abstract]
      ABSTRACT: Digital clubbing is associated with many unrelated serious diseases but its pathogenesis remains a clinical enigma. It has been hypothesized that platelet clusters impacting in the distal vasculature mediate the morphological changes of clubbing. Since the multifunctional cytokines vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) are released on platelet aggregation and are hypoxically regulated, the present study has examined their role in clubbing using immunohistochemistry. Basic fibroblast growth factor (bFGF), transforming growth factor-beta 1 (TGF-beta1), microvessel density, carbonic anhydrase IX (CAIX), hypoxia inducible factor (HIF)-1alpha, and HIF-2alpha were also measured. There was a significant increase in VEGF (p = 0.01), pKDR (p = 0.03), PDGF (p = 0.017), and HIF-1alpha and HIF-2alpha (p = 0.004 and p = 0.004, respectively) expression together with a significant increase in microvessel density (p = 0.03) in the stroma in clubbed digits compared with controls. There was no difference in CAIX (p = 0.25), TGF-beta1 (p = 0.66) or bFGF (p = 0.18) between affected and control groups. These findings suggest that VEGF and PDGF are released after platelet impaction and that their expression is hypoxically enhanced in the stroma after capillary occlusion. VEGF may synergize with PDGF in inducing the stromal and vascular changes present in digital clubbing.
      No preview · Article · Jun 2004 · The Journal of Pathology
    Piotr Kabata

    Go for the same symptoms as in nicotine smoker, as the volatile, active compound do not play a big role in development of clubbing

  • Robert Megerle added an answer:
    Do glycated red blood cells cause vascular tissue damage that leads to atherosclerosis of the heart arteries?

    Could it be that the glycated cells are under such force in the arterial vessels of the heart that plaque builds up quickly in the damaged lumens more rapidly than other arterial vessel locations? It seems to me that a red blood cell that is highly glycated can cause a lot of damage when accelerated at such close proximity of the pressure wave of the left ventricle. A glycated cell cannot slip in between tissues in a normal function and maybe it scratches the lumens along the path to distal locations that have slower circulatory surges (speed in the vessels of circulation). 

    Robert Megerle

    Dr. Bader,

    I thank you and the all the others in helping me to understand what the text I've read have not, when it comes to Glycosylated RB's. In order to help my future clients I must understand the entire cascade of events (effects) of DM. I want to be able to a strong figure in my community as a PCP (small community) that can educate my clients on this growing disease that is much of the time lifestyle induced. I want to be stern as the provider of care in a way that the clients will believe, understand and obey my directions for health nutrition and lifestyles.

  • Ihsan Ates added an answer:
    Is there any consensus about the duration of anticoagulation in case of DVT?

    Is there any consensus about the duration of anticoagulation in case of DVT? specially provoked, unprovoked & recurrent DVT?  

    and when to introduce warfarin, simultaneously or after few days of administration of heparin? 

    Ihsan Ates

  • Ihsan Ates added an answer:
    What are the non invasive methods for carotid stimulation?

    What are the non invasive methods for carotid stimulation?

    Ihsan Ates

  • Ihsan Ates added an answer:
    Any references about angiotensin II receptors?

    I am looking for theory Information about angiotensin II receptors and about their genes, PDF or electronic books. Can you help me?


    Ihsan Ates

  • Nancy Turky asked a question:
    What is the concentration of thrombospondin-1 protein in the serum of acute myocardial infarction patients compared to controls?

    Please if you have an answer I kindly ask you to send me the related article

    Thank you so much

  • Sidharta Chatterjee added an answer:
    What is the evidence-based physiological/pharmacological effect of Beta blocker therapy on renal blood flow and GFR?

    Deterioration of renal function with significant reduction in GFR following treatment with beta blockers have been outlined in clinical practice and experimental research (vide Wilkinson 1982). The beneficial role of dopamine have also been acknowledged, but clinical evidences about the effects of some specific beta blockers are conflicting, i.e., nadolol, propranolol etc. So what's the current guideline of beta blocker usage in patients who have moderate renal impairment?

    Epstein M, Oster JR. Beta blockers and renal function: a reappraisal. J Clin Hypertens 1985; 1: 85-99.

    Sidharta Chatterjee

    Much thanks for your answer Dr. Wesolowski.

    Since Dr. Wesolowski raised the issue of renal artery stenosis, it may be relevant to mention that some drugs including ACEIs are contraindicated in bilateral renal artery stenosis, since that precipitates azotemia (and subsequently uraemia if untreated) due to efferent arteriolar dilation which causes increased BUN, and sodium retention. However, ACEIs can be used as a second line antihypertensives in patients with unilateral renal artery stenosis1. Beta blocker Carvedilol have been successfully used in patients with atherosclerotic bilateral renal artery stenosis2. Again, some experts question the rationality of using ACEIs in renal artery stenosis since they claim that indiscriminate use of ACEIs might increase the risk of cardiovascular death4. Renal artery stenosis stimulates renin release and may raise blood pressure, while beta blockers interfere with renal beta adrenergic receptors (by blocking it) and thus relieving the vasoconstriction (i.e. causing vasodilatation). This reduces GFR, and renal plasma flow, and may lead to sodium retention(??). However, nadolol is an exception which in fact increases effective renal plasma flow3. Is it possible to explain why this (contradictory phenomenon) occurs?





    Best Regards, Sidharta

  • Goran Augustin added an answer:
    LRINEC score for Necrotizing Fasciitis has been in practice for long now but clinically no one is carrying CRP levels in US.Procalc is more imp,why?

    Why are we not replacing CRP levels from LRINEC score with Procalcitonin. Procalc is for sepsis and CRP is for local inflammation. Any rationale that we have to select one over the other. But in LRINEC we can see that we see inflammation by CRP but not sepsis by Procalc, though this score is carried to rule out mortality. 

    Goran Augustin

     Here is the link 

    • Source
      [Show abstract] [Hide abstract]
      ABSTRACT: Fournier's gangrene (FG) is a rapid progressive bacterial infection that involves the subcutaneous fascia and part of the deep fascia but spares the muscle in the scrotal, perianal and perineal region. The incidence has increased dramatically, while the reported incidence of rectal cancer-induced FG is unknown but is extremely low. Pathophysiology and clinical presentation of rectal cancer-induced FG per se does not differ from the other causes. Only rectal cancer-specific symptoms before presentation can lead to the diagnosis. The diagnosis of rectal cancer-induced FG should be excluded in every patient with blood on digital rectal examination, when urogenital and dermatological causes are excluded and when fever or sepsis of unknown origin is present with perianal symptomatology. Therapeutic options are more complex than for other forms of FG. First, the causative rectal tumor should be removed. The survival of patients with rectal cancer resection is reported as 100%, while with colostomy it is 80%. The preferred method of rectal resection has not been defined. Second, oncological treatment should be administered but the timing should be adjusted to the resolution of the FG and sometimes for the healing of plastic reconstructive procedures that are commonly needed for the reconstruction of large perineal, scrotal and lower abdominal wall defects.
      Full-text · Article · Sep 2015 · World Journal of Gastroenterology
  • David C. Ellinsworth added an answer:
    At what percentage of relaxation of acetylcholine to norepinephrine the endothelium of a rat aorta may be considered intact in vitro?

    Recently, someone asked here how to remove the endothelium in a rat aorta. I do agree with all answers. My question now is how to check that the endothelium is correctly removed. In other words, at what percentage of relaxation to norepinephrine or other vasoconstrictors (what concentration?) induced by acetylcholine (also what concentration?) one can consider that the endothelium is correctly removed? Conversely, at what percentage of relaxation one can consider that the endothelium is present or intact?

    David C. Ellinsworth

    And paired data, as you say Dragan, is also very important for organ bath and myograph. I think most don't do it though. Use Bonferroni test also, and your data is pretty much bullet proof

  • Roger Argelio Alvarez added an answer:
    What lines of pulmonary artery smooth muscle cells have given you good cGMP levels in responses sGC activation?

    I am studying pulmonary vascular function and I would like to use cGMP as my readout of NO signaling. My lab is very experienced in doing this in systemic vessels (aortics for example), but I am new to the lab and studying pulmonary biology. When I've tested rat and one line of human PASMC I have gotten poor, barely detectable results. Of note, I am using a commercially available cGMP ELISA Kit from Cell Signaling. As an alternative readout, I will also use pVASP to assess PKG responses. 

    Roger Argelio Alvarez

    Thanks, Jeremy. We currently use 10micrmolar doses of sildenafil. We have also tried using IBMX, as in case there are PDE's other than PDE5 in play. At doses and response times where we generally see robust responses in, say, aortic smooth muscle cells (using a similar number of cells and an identical protocol), we do not get good responses in our pulmonary cells. I have seen that paper where they used porcine vessels, but I have actually (surprisingly) not seen much measuring cGMP in pulmonary smooth muscle cells of other species (human, rat, etc). 

    I am not trying to measure cGMP in snap frozen tissue, just in live cells. 

    Thanks for your suggestion. 

  • Shankar Subramanian added an answer:
    Why is there a site selectivity in atherosclerosis in humans?

    Atheromatous plaques are commonly seen in the coronaries, carotids and aorta. Despite sharing the same risk factors only certain sites are predisposed. Even in the same individual, despite similar blood vessel size, hemodynamic stress and blood flow patterns, plaques are often unilateral and seem to spare vessels sharing similar stress. 

    Why this variation?

    Shankar Subramanian

    Blood flow in a blood vessel is what we can call as a "Complex system". Complex Systems Exhibit Chaotic Behavior that is is characterized by extreme sensitivity to initial conditions, fractal geometry, and self-organized criticality. In a complex system, there are many variables, and they are strongly interdependent. This makes it difficult to know exactly which inputs contribute to an observed output, and the extent of each factor's contributions.

    The concept of sensitive dependence on initial conditions has been popularized in the so-called "butterfly effect": the idea that a butterfly flapping its wings in Brazil could change the weather in Texas. Minute differences in the initial conditions for such a system result in extremely different outcomes.

    The asymmetry observed (whyone vessels gets AS while other does not) in what appears to be almost similar situation is possibly explained by looking at it as a complex system. This article, though not directly related to atherosclerosclerosis, does give an interesting insight on how complex systems work and some of its lessons can be exptrapolated to our situation here.

  • Demian Arturo Herrera Morban added an answer:
    What is a recommended dyslipidemia treatment on a Nephrotic syndrome?

    HMG-CoA inhibitors dont really diminish cholesterol on N-S, and hypertrigliceridemia i havent found proper management of it on N-S, but searching for more information i found ideas of PPAR stimulation and potentiation of HMG-Coa Inhibitors, diminish lipid profile and better outcomes, and using ezetimibe and atorvastatine its better for cholesterol management and atorvastatine with a glitazone improves outcome, also that glitazone tend to protect the kidney, but i havent found studies using ezetimibe plus atorvastatine or simvastatine plus glitazone to try and improve outcome of dyslipidemia on N-S.
    So can the triple therapy of glitazone plus ezetimibe plus atorvastatine or simvastine be used in N-S and would or can improve the outcome of dyslipidemia in N-S.

    Can someone provide additional information, or ideas regarding the hypothetical treatment or some guidelines with information of dyslipidemias on N-S, preventing Cerebral Vascular Diseases.


    Demian Arturo Herrera Morban

    But if its steroid non responser and poor responser to other drugs with some relapses.

  • David C. Ellinsworth added an answer:
    When we add a drug in an isolated 10 ml organ bath must the dilution be not more than 1:20?

    We have Isolated tissue bath, we work on it, herbal, drug blocker....etc

    If our krebs solution in organ is 10 ml, I read paper it said you can not adding more than 0.5 ml , is eqaul to 10.5 ml

    If more than 0.5 all results become ERROR

    Can any one help me ?

    David C. Ellinsworth

    To keep added volumes as low as possible make a stock and serial dilution 1000 fold more concentrated that the start and endpoints of your concentration response curve. For a 10ml organ chamber you will add 10ul of -6 to get 1nM final bath concentration. Then 20ul of -6 to get 3x10(-9), then 7ul of -5 to get -8, then 20ul of -5 to get 3x10(-8), 7ul of -4..... and so on. That way there is minimal change in the volume of the organ chamber..... bearing in mind that you simply can't account for evaporation. As long as you're consistent. 

  • Pablo Salinas added an answer:
    Is there any possibility that contrast agents may trigger the rupture of thoracic aortic dissection (Stanford A type)?

    Actually, I am concerned with the association between the use of contrast agents and rupture of thoracic aortic dissection (Stanford A type).

    Here is the case I experienced recently. A 57-year-old male with a history of hypertension and atrial fibrillation visited our department with a complaint of chest pain. His consciousness was clear and his systolic blood pressure was 100 mmHg. TTE revealed dilated ascending aorta along with moderate aortic regurgitation. Immediately, contrast-CT was performed. Contrast enhanced CT revealed Stanford A type aortic dissection. There was no retention of pericardial effusion. Within a few minutes after that, he fell into CPA. TEE revealed massive retention of pericardial effusion. PCPS was introduced. However, PCPS did not work efficiently probably because of collapse in the right heart. Immediately, pericardial drainage was performed; drainage was not effective because of coagulated blood.

    In this case,

    Should we have performed pericardiotomy to save this patient?

    May contrast agents trigger the rupture of thoracic aortic dissection (Stanford A type)? Actually, I know several cases that thoracic aortic dissection ruptured immediately after contrast CT. I want a paper discussing this point.  

    Pablo Salinas

    Arterial angiograms (i.e. Aortography) may cause progression of an aortic syndrome because of the pressure overload. However, venous injection used for CT studies do not have any direct influence on aortic pressure.

    A mild increase in heart rate and blood pressure may occur because of the contrast per se and anxiety associated to the transfer to radiology. However, in my opinion these effects are modest and the relation to the CT scan is not likely, just the natural evolution of the disease.

    I agree that the only chance in case of pericardial effusion in this setting is to get the patient to emergent sugery

  • Marto Hoary added an answer:
    Vascular stent radial outward force: Which force is needed to make a self-expanding stent grow into the media or adventitia of a vessel?

    Which force is needed to make an implant move/grow through soft tissue? There seems to be a threshold to be overcome by stents (or other implants) to make them grow through tissue. Too low means no growing through. Too high would create lesions. The only reported force I know is from bracelets on the teeth (nearly constant 1-2 N for extraction).

    Is there anything known for soft tissue? Ideally for stents in atrial walls? Which biological processes enable this kind of "growing through"? How could i foster it?

    I'd be thrilled to hear about your input!


    Marto Hoary

    Conventional arterial stents are designed not to grow into the intimal, medial or the adventitial layers. The stent is designed to distribute a uniform radial force sufficient to hold it in place reliably. Restenosis is and undesirable consequence that presents as a growth around the stent. If you want a stent to 'migrate' through the artery wall then it must be designed for that purpose. The form factor and profile for each strut should be reconsidered. Other considerations would be the edge effect of outward radial forces and perhaps other means of constricting the artery to provide a reactive force. These can be mechanically or pharmaceuticaly induced.

  • Carl Taylor added an answer:
    What is the lower end limit on tubing diameter to successfully perform invasive blood pressure measurements in rats?

    Our lab group currently uses a conscious, unrestrained but tethered 275-350g male Wistar rat model of sepsis. As part of this model invasive blood pressure measurements are taken continuously. Currently this is achieved by cannulating the carotid artery with PE-50 tubing, tunnelling the tubing to the nape of the neck and exteriorising through a swivel attached tether system. A blood pressure transducer measures the blood pressure changes by tracking the fluid dynamics within the tubing.

    This surgery required to place this line (and a jugular line to administer fluids) is quite invasive and I would like to reduce the surgical severity if possible. This will likely require choosing more distal cannulation sites where blood vessel diameter is smaller and where the tubing we currently use would be too large. Smaller tubing would therefore be required however I am concerned that smaller tubing will lose patency more easily and/or simply not transmit blood pressure information well enough.

    Does anyone have any advice or experience on this - particularly what the lower limits for tubing diameter for successful blood pressure measurement would be.

    Many thanks.

    Carl Taylor

    As Hubert Dabire commented telemetry really is the best method for monitoring BP. Sure its a little more expensive initially than a tethered system, but overtime you would use far less animals and find much more accurate data from a smaller group size, thus reducing long term study costs. With telemetry subjects are freely moving and you can gain a continuous profile whilst even monitoring more than just the BP, Temperature, Activity, ECG are all possible at the same time from a single device. I know a number of researchers at your facility already carrying out telemetry studies and would be happy to connect you, additionally I'm also available for a more in-depth chat if you would like? Feel free to DM me and I can also share some sepsis paper titles you maybe interested in. 

  • Giuseppe Gatti added an answer:
    What is the rate of bilateral internal thoracic artery (BITA) used at your institution?

    I would like to perform a little survey as the use of BITA grafting formyocardial revascularization.

    Giuseppe Gatti

    Thank you. Please, test the score in your patients or send me the necessary data ( Next, I will perform the analysis according to the models that I attached. Finally, if you agree, we will write a report.

    + 4 more attachments

  • Sergey Gavrilov added an answer:
    When and how do you treat Pelvic Congestion Syndrome? Pelvic Varices?

    What criteria do you use to surgery? Which embolization technique do you use?

    Sergey Gavrilov

    The indication for surgery PCS is symptoms of PCS and expansion and reflux of blood through the gonadal veins. However, up to the end not clear whether it is necessary to do surgery for asymptomatic pelvic varicose veins.

    Embolization gonadal veins - not a reference treatment for PCS. Resection of gonadal veins produces better results at lower cost.

  • Richard Crane added an answer:
    Do you agree that high carbohydrate diet may cause heart problem (cardiovascular disease) ?

    In most of the communities especially are owned by lower socioeconomic status.Diet contains more of carbohydrate than protein and fat. More carbohydrate after catabolism produce more saturated fatty acids. This may disturb the level of LDL( high ) lead to atherosclerosis.

    Richard Crane

    Im Sid, you a right that, for most people, dietary saturated fat, but not cholesterol, affects levels of total cholesterol and LDL. However, certain individuals are "egg sensitive" and experience significantly higher blood cholesterol levels with increased intake of dietary cholesterol. 

  • Roberto Kasuo Miyake added an answer:
    Resilient Telangiectasias: do you search (and treat) the feeder veins?

    We've been removing feeder veins to treat telangiectasis since the 70's. From 2005 on, we've been finding those veins by augmented reality and treating them with CLaCS (a combination of transdermal laser, skin cooling and Dextrose75%).

    The prevalence of those feeder veins is significantly higher in a patient with telangiectasias comparing to a patient with no aesthetic concern on the leg (no visible telangiectasias or small varicosities)

    What is your opinion/experience?

    Roberto Kasuo Miyake

    True Imre Bihari, 

    It is rare to have a simple telangiectasia, disconnected to feeder veins.

    Duplex ultrasound helps to find them.

    VeinLight illumination helps as well but augmented reality (VeinViewer) is the ideal way to diagnose and guide the treatment. 

    Hope to see you in Brazil at IMAP2016! 

    the website is ready

    Best regards


  • Cristina Rodriguez asked a question:
    Has anyone used pluronic gel for in-vivo siRNA delivery in the vascular wall?

    Do you have a detailed protocol?

    Vascular Wall siRNA delivery

  • Jean Noel Fabiani added an answer:
    What size would you consider repairing a descending thoracic aortic aneurysm and why?

    There is no powerful evidence to support any specific threshold. The study reported by the Yale group reported an increase in complications at sizes of 70mm (Davies 2002), but most consensus guidelines suggested repairing them at 55mm. Given the lack of natural history data, what are the arguments for and against this aggressive threshold?

    Jean Noel Fabiani

    It's a difficult question and the answes depends of etiology. In case of Marfan syndrom, I perform on the direct operation (use of stentgraft is forbidden in this pathology)  at 55mm, in case of atherosclerotic aneurysm between 55 and 60 mm, depending of the evoloution. In case of dissecting Aneuvrysm after a diameter of 60mm.Regards.

  • Adeola Michael Gbadebo added an answer:
    Hw can a drug increase left ventricular end-diastolic and end-systolic volumes without reducing ejection fraction

    Does anyone have a rational explanation for how a drug might increase left ventricular end-diastolic and end-systolic volumes without reducing ejection fraction (and without an increase in natriuretic peptides)?

    Adeola Michael Gbadebo

    It could be that the drug has some lusitropic effect while at the same time reducing contractility a little or not changing the contractility at all.

    Please, I need comments on this view I have expressed. 

  • Gabor T Gyenes added an answer:
    Coronary steal due to the large side branch of LIMA; What can we do ?

    41 years old man who had three vessel CABG (LAD-LIMA, RCA-Ao,Cx-Ao) two years ago.

    He had history of recurrent exertional angina, poor exercise tolerance despite maximal medical therapy for the  last six months. Therefore we performed coronary angiography. Angiography showed patent grafts of LAD-LIMA, RCA-Ao, Cx-Ao. However, the  large side branch of LIMA had not been ligated. The side branch can be coronary steal.

    What  we  do ?

    + 4 more attachments

    Gabor T Gyenes

    I agree with all of the above. Other than a coil, you could deploy a covered stent in the LIMA as well, occluding the side branch.

  • Marco Marano added an answer:
    Where can I find references on the alveolar-arterial gradient?

    The Alveolar–arterial gradient (A-aO2, or A–a gradient), is a measure of the difference between the alveolar concentration (A) and the arterial (a) partial pressure of oxygen. It seems an useful and interesting parameter in the topic of pulmonary imbibition, but I failed to find published research in last years.

    Can you help me?

    Marco Marano

    Dear Francesco,

    Many thanks for the paper. I take it just a quick look. 

    I have not yet  the answer to my question. However within the french paper there are some interesting points to read carefully. 

  • Closed account added an answer:
    Should mice die after middle cerebral artery occlusion (MCAO)?

    I'm doing MCAO on mice 22-26 grams using doccol filaments and find that a number of my mice seem to be dying overnight, often the ones that don't die after 24 hours look as if they would not make it to a 2 week time point. I'm not sure why this is. My mice get 1ml of saline IP'ed and are kept in a heating pad at 37 degrees after surgery and get gel and food on the cage floor.

    It seems like I started having problems when I began using laser doppler so maybe I'm causing alot of trauma when placing the probe (I do need to make a fairly large hole in the muscle to get the probe attatched) or it's causing some kind of infection? I want to say there's some connection to when I began using laser doppler but I might be reaching for answers. I've been told my surgery (in terms of inserting the filament) doesn't cause very much trauma.

    Any ideas?


    Thanks, maybe anesthesia is the issue, when I started using laser doppler it takes me a bit to get the probe attached so my surgery is being noticeably prolonged. I'm going to try to lower anesthesia and work on being faster attaching the probe. Hopefully this works.

  • Alessandro Durante added an answer:
    How do you solve this medical problem ?

    Subclavian  Artery  Dissection;  A  Rare Complication of  Transradial  Angiography

    A 52-year-old female patient presenting with typical angina pectoris was admitted to the cardiac catheterization laboratory with evidence of inferior left ventricular wall ischemia detected by myocardial perfusion scintigraphy spect. A short, 6  Fr  sheath was inserted into the right radial artery and a 5 Fr radial diagnostic catheter (Optitorque; Terumo Corporation) and 0.035˝  260 cm 260 cm “J” tip wire were used for diagnostic coronary angiography. While the guidewire was advanced to reach the ascending aorta, there was resistance on the  right subclavian artery. The guidewire was withdrawn and selective right subclavian angiogram was performed that demonstrated the dissection of subclavian artery  (Figure 1).

    Alessandro Durante

    In absence of symptoms I would perform a close monitoring with US and CT. If any worsening is seen I would implant one or more stents to close dissection.

  • Mostafa Samak added an answer:
    Has any one tried to induce Hypertrophy in mouse neonatal cardiomyocytes and measure increase in cell area?

    I have been using primary cultures mouse neonatal cardiomyocytes (NCM) to study hypertrophy. However, the conventional ways of hypertrophy induction (e.g. by catecholamines, Angiotensin II or Endothelin-1) were previously shown to have very subtle effects in mouse compared to rat NCMs (Deng et al., Circ Res. 2000;87:781–788.). I have personally noticed this, and the best results I got were when I used angiotensin, but yet in very high doses (10 -50 micro M) for 48-72 hours. Increase in cell size, being a widely accepted marker, was not more than 10-15%. Moreover, it was shown that mouse NCMs undergo spontaneous hypertrophy without an inducer. Nevertheless, unlike the cited paper, some papers have published better results of up to 1.5 times increase in cell size. I was wondering if there are some tricks that I can utilize to get a more prominent effect.

    Mostafa Samak

    Thank you Nai-Kei for the valuable information.

  • Roberto Flore added an answer:
    What is preclinical carotid atherosclerosis, how is it defined and what is the marker for it?

    Hi, dear all, can you please help me with the follow questions: How to define preclinical carotid atherosclerosis? and what is the marker of it? If carotid intima-media thickness >1mm, may I say this patient already have carotid atherosclerosis, or I should say the patient is in the status of preclinical carotid atherosclerosis?

    Thank you all very much!

    Roberto Flore

    hi Li, could the attached review help you?   

About Vascular Medicine

Vascular medicine (angiology) is the medical specialty which studies the diseases of circulatory system and of the lymphatic system, i.e., arteries, veins and lymphatic vases, and its diseases.

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