I found the article entitled "Leukocyte Accumulation and Hemodynamic Changes in the Cerebral Microcirculation During Early Reperfusion After Stroke" very interesting. It was one of the first studies done on the effect of leukocyte contribution to cerebral ischemia-reperfusion injury by examining both in vivo behavior and microvascular rheology. One thing that i noticed when reading the article was that there were noticeable differences between the leukocyte accumulation in venules versus arterioles. It seems that in the study that was conducted, there was noticeable leukocyte adhesion to the venules in the pial microcirculation of the cortex, but this was rarely observed to happen in the arterioles and capillaries.
The reason this caught my mind is because the study used a technique called MCAO-R, which stands for Middle Cerebral Artery Occlusion and Reperfusion. If the middle cerebral artery is occluded, then why is it that there is only significant leukocyte accumulation in the venules of the microcirculation? After reading the study, I noticed that it commented on the fact that others have gotten similar results, but it did not go on to explain why this happens the way it does. I could just be completely overlooking something really obvious...but i figured i would just put the question out there and see if anybody could come up with an explanation.
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Caveat: I know little about Neurology, and only slightly more about leukocyte movement, so this is a non-specialist's guess, at best.
I do know a little physiology/ histophys, though. Simply from a physical standpoint, the ateries and arterioles are under higher pressure than postcapillary venules. That, and larger arterioles will have sheaths of muscle and elastin fibers surrounding them. So if the venules are (a) under lower pressue and (b) not as thickly coated, it would make them more succeptable to intravasation by migrating leukocytes. I would think that leukocytes would only accumulate at sites where they could leave the blood stream; in a pathological state like ischemia, perhaps the leukocytes are responding to tissue and not vascular damage? Of course, astrocytes encircle vessles in the brain, which likely complicates my simplistic reasoning. So, just a guess.
I was talking to one of the authors of the paper being discussed (http://stroke.ahajournals.org/cgi/content/full/31/5/1153)
and she told me that part of the reason that leukocytes adhere more in the venules than in the arterioles is that:
1)Due to clogging of capillaries, the blood is moving more slowly in the venules, allowing for more rolling and adhesion and,
2)More importantly, the selectins and integrins that the leukocytes use to adhere to the endothelial cells of the vessel have a much greater density in the venules than in the arterioles.
I'm hoping that we will actually see a "blog" from the author soon!
Hi everyone
Im the primary author on this paper. Thanks very much for taking the time to read it and comment on it (even though it might have been required, the postings indicate that you took the time to actually understand the gist of it!)
Your question (do leukocytes adhere to the arteries?) is actually a question I have received in professional meetings/seminars, and is a logical question!
We can also see the arterioles (small arteries, about 70-100um in diameter) in our preparation and almost never see any leukocytes adhering there. There are several reasons we think leukocytes do not adhere to arterioles during reperfusion. First, when the filament is removed from the middle cerebral artery, blood flow is restored to the brain, and blood flow is very robust in the arterioles. The blood "shearing" forces may "whisk away" the leukocytes, preventing them from adhering. As ZoeC mentioned, blood flow in the venules is much slower, giving the leukocytes time to contact and then adhere to the vessel wall. Another reason we think leukocytes dont adhere to arterioles is that these small vessels do not express the ligands (the "docking stations") for the adhesion moclecules that the leukocytes use to adhere ("dock") to the endothelium.
Again, great question!
Heh, at least the "why and where" of leukocyte movement sunk in, if not the mechanism!
BTW, can someone please post what paper we are talking about?
Sorry...I tried to put the url into my earlier comment, but it got covered by this box! It's
Ritter et al. Leukocyte Accumulation and Hemodynamic Changes in the Cerebral Microcirculation During Early Reperfusion After Stroke.Stroke, 2000; 31;1153-1161
thanks!
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