P P Golikov, L M Kozhevnikova, N Iu Nikolaeva, Iu V Arkhipenko
{"title":"[硝苯地平和维拉帕米对失血性休克患者胞浆糖皮质激素受体的影响]。","authors":"P P Golikov, L M Kozhevnikova, N Iu Nikolaeva, Iu V Arkhipenko","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Function of rat liver cytosolic glucocorticoid receptors in the haemorrhagic shock and the effects of verapamil and nifedipine were investigated. Nifedipine administration normalised hepatic receptor functioning affected by the shock. Verapamil administration to animals subjected to shock treatment caused further suppression of the receptor functioning. Both drugs reduced blood corticosterone level in hemorrhagic animals up to control level. Verapramil potentiated hypotension and this deteriorated the course of posthamorrhagic period. This effect may be at least partially attributed to verapramil-induced inhibition of glucocorticoid receptor type II. Nifedipine maintained BP in the subnormal level and reduced the number of animals with the decompensated shock course, which is probably associated with its positive influence on glucocorticoid receptor properties and permits to recommend an introduction of this drug into the complex therapy of the shock.</p>","PeriodicalId":23535,"journal":{"name":"Voprosy meditsinskoi khimii","volume":"48 5","pages":"503-12"},"PeriodicalIF":0.0000,"publicationDate":"2002-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Effect of nifedipine and verapamil on cytosolic glucocorticoid receptors in hemorrhagic shock].\",\"authors\":\"P P Golikov, L M Kozhevnikova, N Iu Nikolaeva, Iu V Arkhipenko\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Function of rat liver cytosolic glucocorticoid receptors in the haemorrhagic shock and the effects of verapamil and nifedipine were investigated. Nifedipine administration normalised hepatic receptor functioning affected by the shock. Verapamil administration to animals subjected to shock treatment caused further suppression of the receptor functioning. Both drugs reduced blood corticosterone level in hemorrhagic animals up to control level. Verapramil potentiated hypotension and this deteriorated the course of posthamorrhagic period. This effect may be at least partially attributed to verapramil-induced inhibition of glucocorticoid receptor type II. Nifedipine maintained BP in the subnormal level and reduced the number of animals with the decompensated shock course, which is probably associated with its positive influence on glucocorticoid receptor properties and permits to recommend an introduction of this drug into the complex therapy of the shock.</p>\",\"PeriodicalId\":23535,\"journal\":{\"name\":\"Voprosy meditsinskoi khimii\",\"volume\":\"48 5\",\"pages\":\"503-12\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2002-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Voprosy meditsinskoi khimii\",\"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":"Voprosy meditsinskoi khimii","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
[Effect of nifedipine and verapamil on cytosolic glucocorticoid receptors in hemorrhagic shock].
Function of rat liver cytosolic glucocorticoid receptors in the haemorrhagic shock and the effects of verapamil and nifedipine were investigated. Nifedipine administration normalised hepatic receptor functioning affected by the shock. Verapamil administration to animals subjected to shock treatment caused further suppression of the receptor functioning. Both drugs reduced blood corticosterone level in hemorrhagic animals up to control level. Verapramil potentiated hypotension and this deteriorated the course of posthamorrhagic period. This effect may be at least partially attributed to verapramil-induced inhibition of glucocorticoid receptor type II. Nifedipine maintained BP in the subnormal level and reduced the number of animals with the decompensated shock course, which is probably associated with its positive influence on glucocorticoid receptor properties and permits to recommend an introduction of this drug into the complex therapy of the shock.