Questions related to Ischemia
Hi Everyone, I want to study the GPCR pathways and their role in ischemic heart disease. Which cardiac cell line would be best for such a study? I was hoping to use H9C2 cells, but people suggested it's challenging to transfect them. Please suggest if people use cell lines for such a study or if there is some other model to study the signaling pathways involved in ischemia. Thank you so much
In the study of myocardial ischemia-reperfusion mechanism, is it necessary to establish a separate ischemia group to compare with the ischemia-reperfusion group? Or just compare the control group to the ischemia-reperfusion group?
I am doing research on ischemia stroke, and I am going to administer 60 mg/kg of Edaravone, which is 3-Methyl-1-phenyl-2-pyrazoline-5-one, to 6 to 7-week-old male ICR mice intraperitoneally. The injection volume is 300 uL.
However, Edaravone (EDRV) has not been dissolved in 0.9% NaCl solution and 100 mM DMSO (Dimethyl sulfoxide) solution.
I prepared 60 mg EDRV in 10 mL of saline and 60 mg EDRV in 10 mL of 100 mM DMSO.
I tried 20-minute sonication, but the sediment is still in the 15 mL conical tube.
Is the concentration of two EDRV solutions too high?
I have photos on them.
Please see my problems, and I am looking forward to your help and advice.
Thank you so much,
My project involves inducing intestinal IRI in mice via occlusion of the superior mesenteric artery (where it branches off the abdominal aorta). After scouring the literature I’ve finally gotten a fairly detailed protocol written up, but cannot find the best approach to isolating and occluding the superior mesenteric artery. If you can provide any resources that may be helpful (tips, papers, and especially videos) I would be very grateful.
I am planing an experiment to figure out the effect of an compound for recovery after stroke.
I am wondering whether sham mice group is necessary for this study.
Some reference didn't use sham or others did it.
In my opinion, only two groups (compound-treated mice and compound-non treated mice after stroke) are enough to demonstrate the effect of the compound.
Will reviewer ask the sham result during paper submission process?
Repurposing of Sodium Thiosulfate (STS) in the treatment of COVID 19 or SARS Cov-2 Viral pandemic of 2019-2020
Repurposing or repositioning of medications to treat emerging diseases is not a new concept; however, I wish to share the story of utilizing sodium thiosulfate (STS) as a repurposed drug in the treatment of calciphylaxis and how even now this drug could possibly assist in the treatment of COVID 19 viral pandemic of 2019-2020 .
Repurposing of STS started out with a paper on vascular ossification calcification that included calciphylaxis in 2005  and subsequent multiple papers regarding the use of STS in the treatment of calciphylaxis [3-7]. Importantly, there have been many other papers dealing with the use of STS in the treatment of calciphylaxis over the years (202 papers in pub med with search terms for sodium thiosulfate and calciphylaxis) and STS is often a part of the multimodal treatment strategy. Recently, 2 days ago, a repurposing of an older malaria drug, hydroxychloroquine, to treat patients with COVID-19 gave me the idea or concept to share this question with an international group of researchers on Research Gate.
Here is a list of other approved medications that are also being considered for repurposing as follows: Tocilizumab - sold under the name Actemra, Kaletra/Aluvia HIV drugs, Hydroxychloroquine as previously mentioned and Remdesivir is a broad spectrum anti-viral medication. There are undoubtedly many more under consideration and are also important in this pandemic crisis.
Sodium Thiosulfate (STS) is a potent antioxidant.
Instead of one unpaired electron as in most antioxidants, STS has (2) unpaired electrons that can be readily donated to sequester reactive oxygen/nitrogen species (RONS). During this chemical reaction process of sequestering RONS, STS also is capable of generating glutathione (GSH) a naturally occurring intracellular antioxidant and thus increases the cellular antioxidant strength in a region actively being damaged (Fig. 1 and 2).
Figure 1. This figure demonstrates the chemical structure of sodium thiosulfate, which is an anti-browning, reducing, and antioxidant agent: Capable of donating electrons to re-pair unpaired damaging electrons to be an effective antioxidant as well as a chelator of cations such as the calcium excess in calcific uremic arteriolopathy – CPLX .
Figure 2. Possible chemical reaction of STS to generate glutathione (GSH) 
Known side effects of sodium thiosulfate (STS) used to treat calciphylaxis
Here is what we know since sodium thiosulfate has become the standard of care in patients with calciphylaxis globally. Obviously, any known allergy to this or a similar sulfur-containing product would preclude its use see references [2-7]. STS may induce an acidosis early-on and with prolonged use could induce osteoporosis see references [2-7].
Sodium Thiosulfate Protective à To Detrimental Cytokine and Reactive Oxygen/Nitrogen Species Storm and Vascular Collapse
Upon initial infection with COVID 19 there is a cauldron of redox chemistry with excessive RONS (the first line of defense against the COVID 19 virus produced by the body’s protective inflammatory response to infection. The cells of immune response include the 1st responder’s neutrophils, mast cells and chronic persistent macrophages - with monocyte migration and monocyte to macrophage transformation at the infectious site of the nasopharyngeal bronchial lining epithelial cells, pneumocytes and capillary endothelial cells.
As these inflammatory cells attempt to clear the virus from these passageway epithelial cell’s they generate RONS with a staggering amount of unpaired reactive oxygen and nitrogen unpaired electrons and toxic cytokines, which over time creates a cytokine storm and RONS beget RONS and cytokines evoke more inflammatory invasion and thus create the cytokine storm. The healthy surrounding cells of the upper and lower pulmonary epithelial, pneumocytes and capillary (blood-oxygen barrier) endothelial cells become a source of collateral damage that originally was intended to result in deleting the invasion of viral envelope DAMPs and PAMPs recognized by these cells in a response to injury and wound healing mechanism to the invading COVID 19 viruses in the pulmonary tissues.
In turn, this RONS storm and cytokine storm leak into the systemic circulation and the protective lining of the endothelial cells (endothelial glycocalyx (ecGCx)) may become damaged and are attenuated and/or lost, which results in a marked increased vascular permeability and loss of intravascular contents into the surrounding extravascular interstitial capillary space. Unfortunately, this loss of intravascular volume due to a ‘capillary leak syndrome’ [8-10] may result in vascular collapse with decreased cardiac output and decreased perfusion of the brain with relative ischemia over time and result in the death of the host or COVID 19 infected patients that have progressed to being on ventilator life support.
Indeed, the COVID 19 virus infection-induced this pulmonary infection with bilateral pneumonia’s requiring ventilator treatment an acute respiratory distress syndrome (ARDS) syndrome (ARDS is an acute inflammatory lung injury, associated with increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue) but these patients actually may be dying of vascular collapse due to a loss of their local and systemic endothelial glycocalyx due to a cytokine and RONS STORM!
In conclusion sodium thiosulfate (STS) would have to be given intravenously; however, these critically ill patients with all have an intravenous established intravenous port to administer medication so it should not be viewed as invasive since these lines are already available. This antioxidant effect might possibly restore some effective endothelial cell function and even re-establish the endothelial glycocalyx or assist in its restoration. The increase in venous or arterial Syndecans may be a key laboratory readout of endothelial glycocalyx loss and systemic vascular collapse . Additionally, patients on ventilators with COVID 19 certainly apply to these thoughts and concepts. The concept of increased pulmonary and possible systemic microvascular permeability is currently a possibility that is not being discussed a great deal at the moment but should be. Further, novel ideas for the prevention of this are of great importance during the COVID 19 pandemic. Drugs that may help to eliminate the excessive RONS with excessive over-reactive cytokines and cytokine storm (such as sodium thiosulfate STS) need to be considered as it relates to capillary leak syndrome with vascular collapse due to viral sepsis of the COVID 19 virus.
1. Xue H, Li J, Xie H, Wang Y. Review of Drug Repositioning Approaches and Resources. Int J Biol Sci. 2018 Jul 13;14(10):1232-1244. doi: 10.7150/ijbs.24612
2. Hayden MR, Tyagi SC, Kolb L, Sowers JR, Khanna R. Vascular ossification-calcification in metabolic syndrome, type 2 diabetes mellitus, chronic kidney disease, and calciphylaxis-calcific uremic arteriolopathy: the emerging role of sodium thiosulfate. Cardiovasc Diabetol. 2005 Mar 18;4:4. Review
3. Hayden MR, Kolb LG, Khanna R. Calciphylaxis and the cardiometabolic syndrome. J Cardiometab Syndr. 2006 Winter;1(1):76-9.
4. Hayden MR. Calciphylaxis and the cardiometabolic syndrome: the emerging role of sodium thiosulfate as a novel treatment option. J Cardiometab Syndr. 2008 Winter;3(1):55-9
5. Hayden MR, Goldsmith D, Sowers JR, Khanna R. Calciphylaxis: calcific uremic arteriolopathy and the emerging role of sodium thiosulfate. Int Urol Nephrol. 2008;40(2):443-51. doi: 10.1007/s11255-008-9373-4. Review.
6. Hayden MR, Goldsmith DJ. Sodium thiosulfate: new hope for the treatment of calciphylaxis. Semin Dial. 2010 May-Jun;23(3):258-62. doi: 10.1111/j.1525-139X.2010.00738.x
7. Sowers KM, Hayden MR. Calcific uremic arteriolopathy: pathophysiology, reactive oxygen species and therapeutic approaches. Oxid Med Cell Longev. 2010 Mar-Apr;3(2):109-21. doi: 10.4161/oxim.3.2.11354. Review.
8. Siddall E, Khatri M, Radhakrishnan J. Capillary leak syndrome: etiologies, pathophysiology, and management. Kidney Int. 2017 Jul;92(1):37-46. doi: 10.1016/j.kint.2016.11.029
9. Colombo R, Wu MA, Castelli A, Fossali T, Rech R, Ottolina D, Cogliati C, Catena E. The effects of severe hemoconcentration on acid-base equilibrium in critically ill patients: the forgotten role of buffers in whole blood. J Crit Care. 2020 Mar 4;57:177-184. doi: 10.1016/j.jcrc.2020.02.016.
10. Bøe OW, Sveen K, Børset M, Druey KM. Raised Serum Levels of Syndecan-1 (CD138), in a Case of Acute Idiopathic Systemic Capillary Leak Syndrome (SCLS) (Clarkson's Disease). Am J Case Rep. 2018 Feb 16;19:176-182. doi:10.12659/ajcr.906514
11. Ranieri VM, Rubenfeld GD, Thompson BT, et al; ARDS Definition Task Force. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012;307(23):2526-2533.
THIS CONCEPT OF REPURPOSING – REPOSITIONING OF MEDICATIONS THAT ARE ALREADY AVAILABLE IS OPEN TO DISCUSSION AND COMMENTS
Sincerely with gratitude,
Melvin R Hayden, MD
Defects in the brain tissue of a rat model I am working with look like small ischemic (not hemorrhagic) strokes when I do H&E stains. I would like to confirm this suspicion by staining the (paraffin-embedded) tissue with some markers. So far I am thinking of a panel using the following: fibrinogen, fibronectin, GFAP for astrocytes. As I'm not familiar with stroke research I'm not sure if there's any common ones I've missed! I would be grateful for any advice.
I am working on ischemic model of hDPSCs. I want to study apoptosis in the cells challenged for different periods of ischemia (3, 6, 12, 24, 48, and 72 h). I am following standard protocols of PI and AO/EtBr staining for the study however not getting the expected results. The bright field imaging showed toxicity in the cells but not in PI and AO/EtBr stained cells. Kindly give your valuable suggestions.
Acute mesenteric ischemia is a syndrome in which inadequate blood flow through the mesenteric circulation causes ischemia and eventual gangrene of the bowel wall .
This seems a bit nonsense question, however I am confused with this. I am doing the middle cerebral artery occlusion experiment using mice using intramural suture (filament) method. As we know the mice face towards the operator and when operator occlude the MCA (of mice) belonging his right side (operator) then it should be the left MCAo of mice, is not it? So the mice should circle (neurological behavior) to the right (left hemisphere impairment affects the function of left body parts). However, in my case when I occlude the right MCAo (my left side mice MCA while operating), the mice circles to the right. So could you explain where the problem is? Either I am doing left MCAo of mice (my left side while operating) or anything else?
What is you take on this statement ?
FFR estimation using CTangiography is a reliable and efficacious noninvasiveimaging modality, as it demonstrates high accuracy in the determination of anatomy and lesion-specific ischemia, which justifies the performance of additional randomized controlled trials to evaluate the clinical benefits of FFRCT guided coronary revascularization.
I have just started using the intraluminal transient MCAO (30min) method in c57BL6 mice. I am thinking of including rotarod testing in my experiments, but have some questions about the protocol. In a paper "Assessing post-stroke behavior in mouse models of focal ischemia" from M. Balkaya et al (2013) they emphasis that pre operative training is important, but they also mention that "if mice are left untrained for several days their score will decline". How often do you need to, or can you test the mice after the surgery? As I understand it, this is most often used for short-term evaluation, but in mentioned paper they say that a difference could be seen as late as 28 days post surgery. Would the results be reliable if the mice were tested once a week (average of 3 trials per time point) for a 4 week period?
Using a mouse model, I will be collecting atrial and ventricular tissues at various ages. I will block the tissues in gelatin and generate 10um sections for immunohistochemistry.
Does anyone have suggestions for what is typically used in the field to identify cardiac dysfunction/ischemia immunohistologically?
I have seen reports that increased levels of Inosine and hypoxanthine occur following acute ischemia preceding increased troponin levels. Additionally, I have seen reports that proNGF increases in ateriols following myocardial infarct. I am new to this area of research and want to proceed properly.
Thank you everyone,
Can there be some other way which can be suggested ?
I use Lagendorff ischemia-reperfusion for rat hears 30 min ischemia then 90 min reprfusion. Half of the hearts did not come back (died) after ischemia. Any reasons for that?
How to stain Myofibroblasts in myocardial infarcted hearts? What about Alpha- Smooth muscle actin in the detection of myofibroblasts? Is there any other specific markers for the detection?
I am currently working on ischemia- reperfusion-induced brain injury in Wistar rats, and as of now we are using Ketamin-Xylazine or low dose of Urethane for inducing anesthesia. I have over heard that these agents could greatly influence the ischemia-reperfusion-induced brain injury and hence looking for better and safe anesthetic agent.
Based on your experience and domain knowledge can any one refer better anesthetic agents for my experiments.
There is currently an issue with ECMO cannulae on the market and limb ischemia. My senior capstone group is curious as to what our target flow should be to prevent this issue. We understand that returning to homeostatic levels with a single insertion point is a lofty goal, so the minimum level gives us a starting point before beginning our concepts.
Recently I am investigating the therapeutic effects of miRNA in ithe cell model of ischemia/re-perfusion injuries. I would like to quantify the levels of target miRNA isolated from ADSCs. Now I have to choose the control group so that the levels of target miRNA could be compared.
Does anyone have any suggestion for how to choose the control group?
i use h2O2 (100uM) for 24 hrs to mimic ischemia model in the cells (cardiomyocytes) . so when i do ROS measurement using DCFH-DA, do i need to add a positive control like ROSUP(solarbio kit) or h2o2 again in my positive control sample? because i have already treated the cells with h2o2 for 24hrs.
(i will use confocal microscope)
I have collected samples from a novel chronic kidney injury model that i am currently studying (as well as control groups).
Rats were sacrificed after several weeks, and kidney tissue samples collected. On the other hand, urine samples were collected weekly.
I will analyse these samples using western blot and other techniques but before this i am considering which loading marker to use.
I have seen that levels of:
- GAPDH can increase with hypoxia
- Ischemia also strongly increases beta-actin and alpha-tubulin expression (PMID: 15464724)
- B-tubulin expression changes with the administration of antineoplastic drugs.
Has anyone got an idea?
Thank you to everyone.
Given that there is no definitive treatment for ischemia, is there a need for positive control in ischemic studies?
Can you use a drug such as Trimetazidine?
i want to make model of global cereberal ischemia reperfusion in rat
so my question is ligation of common carotid artery is enough for induce global cerebal ischemia or i should induce hypotension with bilateral common carotid artery ligation
Hello everyone (my first question on this site)
I am inducing ischemia in H9C2 cardiomyocyte cell line. The overwhelming majority of publications use 95% N2, 5% CO2 gas concentrations for their incubation. Is there a specific reason why CO2 is not used as the main constituent of the gas mixture? Is it due to the fact that CO2 may cause excessive acidity of the media? Would CO2 elicit a different cell response?
Any help would be greatly appreciated.
i came by a research paper the author of which attributed the death of a rat in their experimental group to the re-perfusion method . I myself have been having a very high rat of mortality in my experimental group after MCAO (1 hour ischemia). The mortility is so high thatthe animal did not even qualify the minimum 4 hour reperfusion period for TTC staining.The question is how to minimize the mortility and also that how is the method of reperfusion related to the mortility?
Im doing a I/R model with C2C12 cells and I need to measure ROS production. First I will induce ischemia with the ischemia chamber and then I will measure ROS after 4,6, 8 and 12 hours. In the same timepoints I will induce reperfusion, but I dont know after how many hours after reperfusion its recomendable to measure ROS.
A young male 30 years old healthy BMI 29 ; no comorbid condition presents with superior mesenteric ischemia- what is left is T-colon and Duodenal stump;
On laparotomy; tube duodenostomy is being done; how to manage such a case ??
Prostatic artery embolism is an interventional radiological procedure which can be done on TURP-NON eligible patient for BPH, it involves entrance to Prostatic Artery through the femoral artery- and embolizing w/small bubbly material.
My question is- Due to ischemic necrosis of Hyperplasic prostatic tissue there will be some kind of erosion of that tissue from rest of prostate--is it possible to see that necrotic tissue can block flow of urine- leading an obstruction of urine outflow?
My other question is-- perfusion of pelvic structures are quite complicated and involves lots of small anastomosis'-- after disabling flow of the Prostatic artery, what are the chances of getting bladder neck into an ischemic necrosis--due to possible anastomosis'?
I thank you all for your answers and your comments.
I'm looking at microglial activity, and in some of my sections there is no H&E evidence of neuronal death but there is still microglial activation. I want to stain for neuronal stress to elucidate whether the microglial cells might be responding to a pre-apoptotic environment or if they are activated by the ischemia directly, what stain could I use for paraffin-embedded tissue using dab or fluoro IHC?
i use ketamine/xylazine (110mg/kg and 25mg/kg) for sedation, buprenorphine administered at 0.1mg/kg before surgery and body temp maintained at 37*C during surgery. Most of the mice are dead within 20-30min of ischemia.
All the protocols that i have looked into recommend 2% isoflurane in oxygen, is it a good idea to completely shift to that.
I am currently trying to establish a model of intestinal ischaemia/reperfusion injury in mice, in my lab, with a goal to producing local injury and acute lung injury as a result. However, I am currently having issues with mortality in my I/R animals. My protocol is as follows:
1. Anaesthetise male mice (8 weeks old) with ketamine/xylazine i.p. and transfer to a heated platform.
2. Perform midline incision and laparotomy.
3. Identify superior mesenteric artery. I/R animals have the SMA clamped with a non-crushing surgical occluder for 30-60 minutes (have tried both). Sham animals are treated identically, except for clamping. Ischaemia is confirmed by pallor of the intestines and reflex tachycardia.
4. Gauze is soaked in warm PBS to cover the surgical site for the extent of ischaemia.
5. Clamp is removed to reperfuse the intestines and 1mL of warm PBS is administered i.p. before suturing the muscle and skin walls closed.
6. 30 mg/kg Evans Blue is administered to assess inflammatory oedema secondary to injury.
Mice that underwent 60' ischaemia died at 75 and 90 minutes reperfusion, whilst the sham counterparts survived. Mice that underwent 30' ischaemia died at 45 minutes reperfusion, whilst sham counterparts survived.
Clearly, this is an issue related to the severity of the model, yet so many publications use similar ischaemia/reperfusion timepoints - does anyone have any ideas of where I might be going wrong? I could try and reduce the ischaemic time further, but I risk not inducing a severe enough injury to give me the readouts I need.
Any/all input would be greatly appreciated!
In limb ischemia, after revascularization, some patients suffer from SIRS and MODS. Who plays the major role, ischemia or reperfusion?
2 month old baby after irreversible ischemia of hand waiting for line of demarcation on anti coagulation developed swollen hand with blisters and blackish discoloration of skin to wrist where as dry gangrene of distal fingers,How to differentiate Line of demarcation?
I want to do a research about the the protecting fuction of Nuclear factor-erythroid 2-related factor 2 (Nrf2) in ischemia brain disease.
However, I do not konw what kind of Nrf2 activator and inhibitor we always use？
Can they pass through blood brain barrier and regulating the Nrf2 protein level of brain tissues？
Would you mind telling me which article is the most authoritative one？
Thanks for your great answer！
A new comer of ischemia brain disease.
Some time in case of extensive PAD and critical ischemia we need to perform the simultaneous reconstruction of aorto-iliac and femoral-popliteal segment. What is your opinion about the optimal site of proximal anastomosis for femoral-poplieal bypass with reversed saphenous vein? Should vein takes-off from the synthetic graft or from the common femoral (femoral) artery? Some surgeons claimed against the anastomosis between synthetic material and vein.
There appears to be a low dose therapeutic window for alpha lipoic acid in both schizophrenia and ischemia reperfusion. Could disturbances in glutathione homeostasis, either through increased synthesis or reduced degradation be a factor? The half-life for both alpha lipoic acid and glutathione is very short.
There was already a significant difference in the infarct size. The ischemia time was 30 min, followed by 24 hours of reperfusion.
I want to compile a list of acute pathological or physiological events that last no more than 5 min. Currently, I can only think of cortical spreading depression (CSD) and seizure that qualify for this standard (very short, duration less than 5 min). Status epilepticus maybe OK, but I still think it lasts too long. Ischemia is not qualified for the same reason.
Can some one give me more examples? Any physiological and pathological events will be fine, as long as they occur acutely and are short-lived.
I am operating mice to induce ischemia in the left hindlimb by ligating the femoral artery. The procedure is well established i our laboratory and after three years of working on the project I might say we got quite experienced with it.
However, recently we see that mice of one certain genotype develop swelling of the right (=not operated) hindlimb. Infection is not likely, as the rest of the mice (operate leg, eyes, etc) are not inflammated, red, or swollen...
Does anyone has an idea what might be the reason of this swelling?
Recanilization of the occluded vessel is guided by the state of perffused territory. In acute state recanalization is warrented within limited theraputic window. What about in cases of chronic ischemia or acute ischamia in setting of chronic occlusion?
I'm having trouble finding papers that clearly point out what exactly induces apoptosis in macrophages after ischemia and its effects, later on, on the failing heart.
Any links to papers would be greatly appreciated.
I have tried the procedure with suggested protocol in 24 hrs Transient Focal cerebral ischemia in rats. Im not getting proper results even the animal shows severe lesion symptoms on 24hrs. Any suggestions or modification in the available protocol will be helpful for me.
Thank U in advance
When I expose my primary cortical neurons to hypoxia(1%) in a professional hypoxic workstation, only about 10% of the cells die at 24 hrs. Even at 48 hrs, it just reaches up to 20%-30%. Is it normal? Should it be that neurons are more susceptible to hypoxia? Thanks~
Two years ago, Zhang et al. found mitophagy or autophagy for mitochondria is protective in the reperfusion phase, while deleterious in the earlier ischemia phase. But at that time, seemingly they didn't give explicit explanation for that discrepency. So recently I wonder, to date is there any attempt to unravel the puzzle?
Thank you in advance.
Can anyone kindly suggest me about suitable in-vitro model to study ischemia. I tried with neuro-2a cell lines by inducing apoptosis by various concentration of cocl2. it induced apoptosis but i could not found up-regulation of any related gene (TNF-a, Fas). I want to make a in-vitro ischemia model to study Fas mediated apoptosis and want to check my developed fas targeting peptide. Kindly suggest me about cell line and developed protocol.
I've found various different paper which used I/R protocols in H9c2 cells to bring those cells into apoptosis, but none worked in my lab so far. Additionally, I've found none where they tested the anti-apoptotic effect of insulin after/during I/R in vitro.
Hope you can help me
i would like to know the best way to track down neurogenesis spatiotemporally in my samples, please suggest the best method? which is the best method?
When intestinal tissue is analyzed for IFABP it appears to us as a very nice band at 15kDa, but always shows an "exactly" 30kDa band when serum is analyzed for western blot (and nothing else below this size). Do you have any idea what this means? the IFABP should be released into serum after intestinal ischemia (normally evaluated by ELISA), but in serum we find this higher band. Thank you!
I am having TP, TN, FP and FN for detected and classified ST segments for detection of ischemia in ECG signals
Would you advise against use of cortical or whole brain slices for in vitro I/R studies? Why?
Failed endopyelotomy can be due to irreparable pelvi-caliceal system,puj ischemia with restenosis, anastomotic leak with urinoma and fibrosis.
My understanding is, when the myocadium cells lack of blood supply, the cell will be damaged but to some degree, it's still reversible. When the blood flow recovered, the cell can become alive again. When the ischemia is serious to a certain stage, the cell will die completely. Thus even the blood flow recover, the cell cannot gain live again, call irresversible. (if these are not true, please kindly correct me)
And my question is, for a specific patient, how to judge if his ischemia is reversible, irreversible? E.g. by using some imaging machines??
This situation has been plaguing our lab for some time. When exposing hippocampal slices to ischemia either they recover fully or develop an injury potential and do not recover at all?
There is very few data on how to manage these lesions, but the thromboembolic potential seems to be high, namely visceral and renal artery ischemia. Do you think we should preemptive treat these patients?
Intravenous thrombolysis is an effective treatment of ischemic stroke, if administered within 4.5 hours from outcome. Since sudden hearing loss is probably due to cochlear ischemia, intravenous thrombolysis within 4.5 hours from onset of deafness should be effective in this condition, too.
Simple question: Are there any published studies regarding the clinical benefit of I.v. tPA in ischemia stroke in a population based on proven vascular occlusion (e.g. By CTA). All the initial placebo control studies needed only a non contrast CT and therefore the site or the mere existence of a vascular occlusion was not shown. Thank you
I am studying gender differences following cerebral ischemia, and i have surprisingly noted that NSPCs donot express BDNF after 7 days of ischemia. I performed IHC and co localization studies with Brdu . Has anybody seen the same expression pattern of BDNF?
I am working in cerebral ischemic models. I generally used in vivo models in mice or rat for the ischemia induction. I am also interested in in vitro ischemic models such as OGD-R. Would be very grateful if anybody could provide me the detail of the ogd protocol.
As it is obvious that the level of TNF-alpha is increased following cerebral ischemia. I am going to perform the immunostaining for TNF-alpha positive cells in mice brain sections which is challenged with MCAo induced focal cerebral ischemia. I am going to use the DAB substrate for this purpose. Could anybody provide me the detailed protocol for this purpose?
Recently, I take use of microdialysis to measure glutamate in ischemia, the probe is put in the center of the striatum of mice, but no rise is seen after ischemia as papers have showed. I did not clear the oxygen from the ACSF, which is used in electrophysiology.
I found a protocol that uses a single dose heparin in hepatic ischemia reperfusion injury induction, I wonder if it`s applicable in the small intestine.
Iba 1 is used for the immunohistochemical analysis of activated microglial cells. I am doing stroke animal research and frequently encounter the staining with the Iba 1 antibody. My problem is Iba 1 stains both MCAo operated slices (suggesting the over expression of microglia in ischemia) and the sham operated slices also (though the morphology of the iba 1 positive cells from sham and MCAo are completely different.) I used both DAB substrate or immunofluoroscence for the Iba cells and got the same result. How can I eliminate the Iba 1 positive cells in sham operated (or normal) mice brain slices?