Blood flow through cerebral collateral vessels one month after middle cerebral artery occlusion.

Abstract

Acute occlusion of a middle cerebral artery (MCA) reduces cerebral blood flow in normotensive Wistar-Kyoto rats (WKY) and in stroke-prone spontaneously hypertensive rats (SHRSP). The goal of this study was to determine whether MCA occlusion produces a sustained reduction in cerebral blood flow or whether collateral vessels restore blood flow to normal levels. We measured blood flow through cerebral collateral vessels to the territory of the occluded MCA and to homologous tissue of the other hemisphere in WKY 1 month after occlusion of the MCA. Cerebral blood flow, measured with mkrospheres, was restored to normal levels under control conditions in the territory of the occluded MCA. During vasodilatation produced by seizures, blood flow and vascular conductance were increased to similar levels in tissue distal to the site of MCA occlusion and in the homologous tissue of the other hemisphere. MCA occlusion did not produce infarction in any of the WKY. In contrast, 1 month after MCA occlusion in SHRSP, a large atrophic infarct was invariably present in the territory of the occluded MCA. The number of collateral vessels to the territory of the MCA do not differ in SHRSP and WKY. Internal diameter and orientation of the anastomotic vessels differ in SHRSP and WKY. We conclude that, after 1 month of MCA occlusion, changes in the collateral vessels supplying the territory of the occluded MCA in WKY were sufficient to restore blood flow to normal under control conditions and to virtually normal levels during vasodilatation. We suggest that, in normotensive rats, protection against infarction after occlusion of the MCA may relate, at least in part, to effective dilator reserve in collateral vessels. (Stroke 1987;18:407-411) D STAL branches of the 3 major cerebral arteries anastomose to form an extensive collateral network in rats.12 Occlusion of the middle cerebral artery (MCA) increases the diameter of these anastomoses 34 and, in 5-week-old normotensive Wistar-Kyoto rats (WKY), occlusion of the MCA does not produce infarction.3 In contrast to WKY, in strokeprone spontaneously hypertensive rats (SHRSP), major cerebral vessels are smaller in lumenal diameter, 6 cerebral vascular resistance is greater, 7 and occlusion of the MCA produces infarction. 3Five minutes after MCA occlusion, blood flow through collateral vessels to the territory of the occluded MCA is significantly less in SHRSP than in WKY.8 Furthermore, vasodilatation produced by seizures after MCA occlusion produces minimal increases in blood flow to the territory of the occluded MCA in SHRSP and WKY. If the anastomoses in Received March 21, 1986; accepted October 14, 1986. WKY enlarge progressively after occlusion of the MCA, 34 blood flow through the collateral vessels should increase toward normal levels and if sufficient, protect tissue distal to the occlusion from infarction.In this study, we measured blood flow through cerebral collateral vessels in WKY after 1 month of MCA occlusion. Flow was measured during control conditions and during vasodila...

High NaCl predisposes Dahl rats to cerebral infarction after middle cerebral artery occlusion.

“…8 After 1 month of MCA occlusion in WKY, blood flow and collateral reserve are virtually normal and tissue infarction is absent. 10 In SR/Jr fed a low NaCl diet and normotensive SS/Jr of the present study, collateral protection from infarction usually followed occlusion of the MCA. Thus, in normotensive control rats, including WKY, 210 Wistar,*-12 SpragueDawley, 5 SS/Jr, and SR/Jr, fed a low NaCl diet, the final outcome is a developed collateral supply that most often protects tissue from infarction in the cortical territory of the occluded MCA.…”

Effects of Nitric Oxide Synthase Inhibition on Cerebral Blood Flow following Bilateral Carotid Artery Occlusion and Recirculation in the Rat

“…Certain strains of rat (e.g., Wi star) are known to be resistant to ischemia induced by cerebrovascular occlusive procedures owing to the presence of an effective vasodilator reserve in the collateral ves sels (Coyle and Heistad, 1987). In contrast, the spontaneously hypertensive strain of rat is more susceptible than its normotensive counterparts to ischemic cerebral damage following acute occlusion of a major cerebral artery (Coyle, 1984;Ginsberg and Busto, 1989).…”

“…Induction of bilateral ca rotid occlusion (BCO) in L-NAME-treated animals re sulted in a reduction of cCBF to 30% of baseline. During recirculation subsequent to 20 min of BCO, cCBF in An important intrinsic mechanism for limiting cellular damage following cerebral ischemia is that of collateral channel activation (Chen et aI., 1986;Coyle, 1986; Brint et aI., 1988;Hossmann, 1988).Certain strains of rat (e.g., Wi star) are known to be resistant to ischemia induced by cerebrovascular occlusive procedures owing to the presence of an effective vasodilator reserve in the collateral ves sels (Coyle and Heistad, 1987). In contrast, the spontaneously hypertensive strain of rat is more susceptible than its normotensive counterparts to ischemic cerebral damage following acute occlusion of a major cerebral artery (Coyle, 1984;Ginsberg and Busto, 1989).…”

Adeno-associated viral vector-mediated hypoxia-regulated VEGF gene transfer promotes angiogenesis following focal cerebral ischemia in mice

“…The function of newly formed microvessels in the adult brain after stroke is uncertain. [8][9][10][11][12] The concerted action of many angiogenic molecules is needed in this process, in which VEGF is the most important molecule in each step of angiogenesis. 13,14 Controlling VEGF expression and maintaining a certain level of VEGF in the ischemic region appear to be crucial for focal angiogenesis.…”