{"title":"Microvascular changes during cerebral ischemia and reperfusion.","authors":"G J del Zoppo","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Although the microvascular compartment contributes significantly to intravascular volume, its importance to disease is often underestimated. Events surrounding cerebral ischemia and recent interest in strategies which may lead to cerebral artery reperfusion in thrombotic or embolic stroke have raised enquiries about the role(s) the microvasculature may play during ischemia and reperfusion. Except in a few instances, little is known about the organization of the microvasculature in cerebral tissue. However, it is apparent that ischemia, inflammatory insults, and infectious processes affect the cerebral microvascular endothelia, cellular elements of the circulating blood compartment, and hemostasis. The precise mechanisms are under study. Observations in isolated microvascular systems from brain tissue, direct visualization of the pial cortical vasculature, and in situ preparations which allow study of the subcortical microvasculature have added to our understanding of these processes. During focal cerebral ischemia and reperfusion alterations of endothelial cell reactivity, coagulation system activation, and granulocyte-endothelial cell interactions are a few of the events affecting microvascular integrity which have been documented. Oxygen free radical generation, selectin and integrin expression and intercellular adhesion, vasomotor responses, endothelial permeability changes, and coagulation system and platelet activation are some of the microvascular processes currently under study which appear to be triggered during ischemia and reperfusion. In view of these events the responses of the cerebral microvasculature to ischemic injury remain relatively unexplored.</p>","PeriodicalId":9739,"journal":{"name":"Cerebrovascular and brain metabolism reviews","volume":"6 1","pages":"47-96"},"PeriodicalIF":0.0000,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cerebrovascular and brain metabolism reviews","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Although the microvascular compartment contributes significantly to intravascular volume, its importance to disease is often underestimated. Events surrounding cerebral ischemia and recent interest in strategies which may lead to cerebral artery reperfusion in thrombotic or embolic stroke have raised enquiries about the role(s) the microvasculature may play during ischemia and reperfusion. Except in a few instances, little is known about the organization of the microvasculature in cerebral tissue. However, it is apparent that ischemia, inflammatory insults, and infectious processes affect the cerebral microvascular endothelia, cellular elements of the circulating blood compartment, and hemostasis. The precise mechanisms are under study. Observations in isolated microvascular systems from brain tissue, direct visualization of the pial cortical vasculature, and in situ preparations which allow study of the subcortical microvasculature have added to our understanding of these processes. During focal cerebral ischemia and reperfusion alterations of endothelial cell reactivity, coagulation system activation, and granulocyte-endothelial cell interactions are a few of the events affecting microvascular integrity which have been documented. Oxygen free radical generation, selectin and integrin expression and intercellular adhesion, vasomotor responses, endothelial permeability changes, and coagulation system and platelet activation are some of the microvascular processes currently under study which appear to be triggered during ischemia and reperfusion. In view of these events the responses of the cerebral microvasculature to ischemic injury remain relatively unexplored.