{"title":"缺血再灌注和细胞膜功能障碍。","authors":"M O Perry, G Fantini","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>One to 3 hours of partial skeletal muscle ischemia-reperfusion in dogs and rats causes cell membrane depolarization. Intracellular levels of adenosine triphosphate remain normal, suggesting that direct membrane injury rather than electrogenic pump failure occurs. Membrane depolarization can be prevented by superoxide dismutase and catalase, or by neutrophil depletion. Oxygen free radicals may be one type of mediator causing membrane damage, and it appears that leukocytes release these toxic species.</p>","PeriodicalId":18718,"journal":{"name":"Microcirculation, endothelium, and lymphatics","volume":"5 3-5","pages":"241-58"},"PeriodicalIF":0.0000,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Ischemia-reperfusion and cell membrane dysfunction.\",\"authors\":\"M O Perry, G Fantini\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>One to 3 hours of partial skeletal muscle ischemia-reperfusion in dogs and rats causes cell membrane depolarization. Intracellular levels of adenosine triphosphate remain normal, suggesting that direct membrane injury rather than electrogenic pump failure occurs. Membrane depolarization can be prevented by superoxide dismutase and catalase, or by neutrophil depletion. Oxygen free radicals may be one type of mediator causing membrane damage, and it appears that leukocytes release these toxic species.</p>\",\"PeriodicalId\":18718,\"journal\":{\"name\":\"Microcirculation, endothelium, and lymphatics\",\"volume\":\"5 3-5\",\"pages\":\"241-58\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1989-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Microcirculation, endothelium, and lymphatics\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Microcirculation, endothelium, and lymphatics","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Ischemia-reperfusion and cell membrane dysfunction.
One to 3 hours of partial skeletal muscle ischemia-reperfusion in dogs and rats causes cell membrane depolarization. Intracellular levels of adenosine triphosphate remain normal, suggesting that direct membrane injury rather than electrogenic pump failure occurs. Membrane depolarization can be prevented by superoxide dismutase and catalase, or by neutrophil depletion. Oxygen free radicals may be one type of mediator causing membrane damage, and it appears that leukocytes release these toxic species.
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