When performed experimentally for stroke/ischemia/reperfusion models, does MCAO completely prevent blood flow to the occluded side or just significantly reduce it by cutting off the main source? Or to rephrase, are there redundant mechanisms/vessel pathways in the rodent brain that supply at least some blood flow to the occluded side during MCAO?
Hello Jordan,
If you are doing the occlusion by microfilament technique, the idea is that it blocks complety the blood flow into the MCA. Howerver in our studies I have seen that there are some diferences in the vascularization, and in some animals this brain terretory can be perfused by other very small vessels. I think that one think you can do is meassure with doppler laser the blood flow drop during the surgery (or with other mothods if you have them available), and then make some anatomical studies to determine the size of your infarc and the size of the penunbra (the region that surrounding the ischemic core). In this mice that have additional vascularization you can note differences between the sizes and location of ischemic the core and penunbra. But you can be sure that the territory of the MCA will be completly occuded (and leds the tissue necrosis) if you perform the right technique and use the filament to do it (we use #22), and the other little ways (if there) are not significantly important.
Whenever we do transient middle cerebral artery occlusions, we use a laser doppler to measure blood flow (as mentioned above). We look for a reduction of blood flow, less than 70% of the initial blood flow (which will vary some from mouse to mouse). So an occlusion is defined not as a total loss of blood flow but reduced blood flow. That being said, there's definitely some variability from strain to strain with mice and rats. I recommend looking at this article http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2949237/ for some specific details regarding strain differences in vasculature. To quote directly from the article, "the gross anatomy of the circle of Willis, the role of communicating arteries, collateralization, and anastomotic connections within the MCA and with adjacent vascular territories", all of which vary slightly, will all affect the severity of the MCAO. That article provides a lot of specific strain information that might help you out.
Hi Jordan, MCA occlusion prevents blood from going through the MCA and its downstream branches, but you can still get perfusion through collateral vessels (anastomoses with other cerebral vessels; e.g., the ACA. Strain differences are in part related to the richness of these anastomoses.
Wonderful, thank you all for your responses. Very informative and helpful
In 1977 I defend my PhD-thesis on the study of measurement of blood flow in the pig by means of the in those days popular Xe-133 clearance technique.. I found a lot of sources of error in this technique. Nowadays much better techniques are available. One striking thing I found was that when heart function was arrested the clearance continued for some time indicating the maintenance of a low cerebral flow. One explanation of this phenomenon I gave was propulsive activity of the bloodvessels. I named this way of perfusion without arterial blood pressure autoperfusion. I have not further investigated this phenomenon and I am not aware of publications about it. I am very interesting in your ideas and experiences.
Wim van Duyl
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