{"title":"缺血诱导的脑细胞损伤机制。膜理论。","authors":"K Kogure, J Tanaka, T Araki","doi":"10.1007/BF03160360","DOIUrl":null,"url":null,"abstract":"<p><p>Temporal ischemia of the brain injures only the selectively vulnerable brain cells. The dying process evolves along with glutamate-mediated intracellular signal-transduction system, together with a loss of Ca2+ homeostasis. Such post-ischemic changes eventually disrupt functional and structural integrity of the cell membrane and kill the neuron. Molecular basis in pharmacoprotective agents is discussed.</p>","PeriodicalId":77753,"journal":{"name":"Neurochemical pathology","volume":"9 ","pages":"145-70"},"PeriodicalIF":0.0000,"publicationDate":"1988-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF03160360","citationCount":"49","resultStr":"{\"title\":\"The mechanism of ischemia-induced brain cell injury. The membrane theory.\",\"authors\":\"K Kogure, J Tanaka, T Araki\",\"doi\":\"10.1007/BF03160360\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Temporal ischemia of the brain injures only the selectively vulnerable brain cells. The dying process evolves along with glutamate-mediated intracellular signal-transduction system, together with a loss of Ca2+ homeostasis. Such post-ischemic changes eventually disrupt functional and structural integrity of the cell membrane and kill the neuron. Molecular basis in pharmacoprotective agents is discussed.</p>\",\"PeriodicalId\":77753,\"journal\":{\"name\":\"Neurochemical pathology\",\"volume\":\"9 \",\"pages\":\"145-70\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1988-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1007/BF03160360\",\"citationCount\":\"49\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neurochemical pathology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1007/BF03160360\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurochemical pathology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/BF03160360","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The mechanism of ischemia-induced brain cell injury. The membrane theory.
Temporal ischemia of the brain injures only the selectively vulnerable brain cells. The dying process evolves along with glutamate-mediated intracellular signal-transduction system, together with a loss of Ca2+ homeostasis. Such post-ischemic changes eventually disrupt functional and structural integrity of the cell membrane and kill the neuron. Molecular basis in pharmacoprotective agents is discussed.
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