{"title":"大鼠MCA闭塞再循环模型中LCGU和rCBF的变化及新型自由基清除剂MCI-186的改善作用。","authors":"S Yuki, K Kogure","doi":"10.1007/BF02815171","DOIUrl":null,"url":null,"abstract":"<p><p>We examined the change of regional cerebral blood flow (rCBF) and local cerebral glucose utilization (LCGU) in the middle cerebral artery (MCA) occlusion or recirculation model of rats, and tested anti-ischemic effects of a free radical scavenger, 3-methyl-1-phenyl-pyrazolon-5-one (MCI-186). A remarkable increase in LCGU was observed in the cortex supplied by the anterior cerebral artery after recirculation. This hypermetabolism of glucose was at least partly caused by the postischemic oxidative injury, since MCI-186 ameliorated the high LCGU in this area. These results suggested the usefulness of this type of free radical scavenger for inhibiting the postischemic injury.</p>","PeriodicalId":18736,"journal":{"name":"Molecular and chemical neuropathology","volume":"32 1-3","pages":"123-8"},"PeriodicalIF":0.0000,"publicationDate":"1997-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02815171","citationCount":"2","resultStr":"{\"title\":\"The changes of LCGU and rCBF in the MCA occlusion-recirculation model in rats and the ameliorating effect of MCI-186, a novel free radical scavenger.\",\"authors\":\"S Yuki, K Kogure\",\"doi\":\"10.1007/BF02815171\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>We examined the change of regional cerebral blood flow (rCBF) and local cerebral glucose utilization (LCGU) in the middle cerebral artery (MCA) occlusion or recirculation model of rats, and tested anti-ischemic effects of a free radical scavenger, 3-methyl-1-phenyl-pyrazolon-5-one (MCI-186). A remarkable increase in LCGU was observed in the cortex supplied by the anterior cerebral artery after recirculation. This hypermetabolism of glucose was at least partly caused by the postischemic oxidative injury, since MCI-186 ameliorated the high LCGU in this area. These results suggested the usefulness of this type of free radical scavenger for inhibiting the postischemic injury.</p>\",\"PeriodicalId\":18736,\"journal\":{\"name\":\"Molecular and chemical neuropathology\",\"volume\":\"32 1-3\",\"pages\":\"123-8\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1997-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1007/BF02815171\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular and chemical neuropathology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1007/BF02815171\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular and chemical neuropathology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/BF02815171","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The changes of LCGU and rCBF in the MCA occlusion-recirculation model in rats and the ameliorating effect of MCI-186, a novel free radical scavenger.
We examined the change of regional cerebral blood flow (rCBF) and local cerebral glucose utilization (LCGU) in the middle cerebral artery (MCA) occlusion or recirculation model of rats, and tested anti-ischemic effects of a free radical scavenger, 3-methyl-1-phenyl-pyrazolon-5-one (MCI-186). A remarkable increase in LCGU was observed in the cortex supplied by the anterior cerebral artery after recirculation. This hypermetabolism of glucose was at least partly caused by the postischemic oxidative injury, since MCI-186 ameliorated the high LCGU in this area. These results suggested the usefulness of this type of free radical scavenger for inhibiting the postischemic injury.
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