{"title":"Blood-damaged tissue interaction in experimental brain ischemia.","authors":"J M Hallenbeck","doi":"10.1007/978-3-7091-9334-1_62","DOIUrl":null,"url":null,"abstract":"<p><p>This paper is a review and synthesis of work done in our laboratory by many investigators over roughly 18 years dealing with the microcirculation in a zone of acute ischemic injury. The work has been guided by a hypothesis that blood flowing through the microcirculation of an acute injury zone is capable of undergoing a multifactorial interaction at the blood-endothelial interface that can progressively impair microvascular perfusion and contribute locally to the evolution of cellular damage and death. Our work has implicated Factor VIII/von Willebrand factor, prostanoids, leukocytes, platelets, platelet-activating factor, leukotrienes, adhesion receptors, monocytes/macrophages, and cytokines in this interaction.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"233-7"},"PeriodicalIF":0.0000,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"14","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta neurochirurgica. Supplementum","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/978-3-7091-9334-1_62","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 14
Abstract
This paper is a review and synthesis of work done in our laboratory by many investigators over roughly 18 years dealing with the microcirculation in a zone of acute ischemic injury. The work has been guided by a hypothesis that blood flowing through the microcirculation of an acute injury zone is capable of undergoing a multifactorial interaction at the blood-endothelial interface that can progressively impair microvascular perfusion and contribute locally to the evolution of cellular damage and death. Our work has implicated Factor VIII/von Willebrand factor, prostanoids, leukocytes, platelets, platelet-activating factor, leukotrienes, adhesion receptors, monocytes/macrophages, and cytokines in this interaction.