M Haida, Y Shinohara, M Yamamoto, T Nagayama, D Kurita
{"title":"The effect of BAY K-8644 on cytotoxic edema induced by total ischemia of rat brain.","authors":"M Haida, Y Shinohara, M Yamamoto, T Nagayama, D Kurita","doi":"10.1007/978-3-7091-9334-1_78","DOIUrl":null,"url":null,"abstract":"<p><p>The calcium channel activator BAY K-8644, a dihydropyridine (DHP) derivative, has been shown to possess neurochemical and behavioral activities, but its effect on ischemic brain damage has remained unknown. This report describes the effect of the drug on the progression of cytotoxic edema induced by total ischemia of the brain, evaluated by measuring the time constant, k, of elongation of the 1H-NMR relaxation time (T2) after brain biopsy. Twenty-six male Wistar rats were divided into four groups, (a) control (saline) group (n = 10), (b) BAY K-8644 vehicle group (n = 4), (c) BAY K-8644 0.03 mg/kg group (n = 6) and (d) BAY K-8644 0.3 mg/kg group (n = 6). The k value of group (d), 18.2 +/- 5.8 min (mean +/- SD), was significantly higher compared with those of groups (a) 10.3 +/- 1.6, (b) 11.8 +/- 1.5 and (c) 9.8 +/- 3.3 min (p < 0.01 by ANOVA). These results indicate that BAY K-8644 delayed the progression of cytotoxic edema induced by total ischemia of the rat brain.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"293-5"},"PeriodicalIF":0.0000,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta neurochirurgica. Supplementum","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/978-3-7091-9334-1_78","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
The calcium channel activator BAY K-8644, a dihydropyridine (DHP) derivative, has been shown to possess neurochemical and behavioral activities, but its effect on ischemic brain damage has remained unknown. This report describes the effect of the drug on the progression of cytotoxic edema induced by total ischemia of the brain, evaluated by measuring the time constant, k, of elongation of the 1H-NMR relaxation time (T2) after brain biopsy. Twenty-six male Wistar rats were divided into four groups, (a) control (saline) group (n = 10), (b) BAY K-8644 vehicle group (n = 4), (c) BAY K-8644 0.03 mg/kg group (n = 6) and (d) BAY K-8644 0.3 mg/kg group (n = 6). The k value of group (d), 18.2 +/- 5.8 min (mean +/- SD), was significantly higher compared with those of groups (a) 10.3 +/- 1.6, (b) 11.8 +/- 1.5 and (c) 9.8 +/- 3.3 min (p < 0.01 by ANOVA). These results indicate that BAY K-8644 delayed the progression of cytotoxic edema induced by total ischemia of the rat brain.
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