[Effect of nifedipine and verapamil on cytosolic glucocorticoid receptors in hemorrhagic shock].

Voprosy meditsinskoi khimii Pub Date : 2002-09-01
P P Golikov, L M Kozhevnikova, N Iu Nikolaeva, Iu V Arkhipenko
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Abstract

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.

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[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]。
研究了出血性休克大鼠肝细胞内糖皮质激素受体的功能及维拉帕米和硝苯地平的作用。硝苯地平使受休克影响的肝受体功能恢复正常。维拉帕米给予休克治疗的动物可进一步抑制受体功能。两种药物均可使出血性动物的血皮质酮水平降至对照水平。维拉普兰增强低血压,这恶化了出血后时期的进程。这种作用可能至少部分归因于维拉普兰诱导的糖皮质激素受体II型抑制。硝苯地平将血压维持在亚正常水平,并减少了失代偿性休克过程的动物数量,这可能与它对糖皮质激素受体特性的积极影响有关,并允许推荐将这种药物引入休克的综合治疗中。
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