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家兔内毒素性发热与利血平退热作用关系的研究(作者译)

[Studies on the relationship between the endotoxin induced fever and the antipyretic effect of reserpine in rabbits (author's transl)].

作者信息

Kanoh S, Nishio A

出版信息

Nihon Yakurigaku Zasshi. 1979 Sep;75(6):527-33.

PMID:317268
Abstract

It has been well documented that fever could be mediated with endogenous pyrogen released from reticuloendothelial system(RES) by administration of bacterial endotoxin(LPS) intravenously to rabbits. On the contrary, reserpine which has various pharmacological activities by depleting catecholamines decreases the normal body temperature as well as endotoxin induced fever. In this paper, we focussed our attention on the effect of reserpine on the production of endogenous pyrogen with relation to the antipyretic effect in endotoxin fever and obtained the following results: Endogenous pyrogen could be detected by intravenous administration of LPS(0.5 micrograms/kg) during the fever. However, endogenous pyrogen was undetectable with intracisternal administration of LPS(0.01 microgram/body) which provoked long-lasting fever. Reserpine (1 mg/kg, i.v.) decreased both body temperature induced by intracisternal administration of LPS(0.01 microgram/body) or intravenous administration of LPS(0.5 microgram/kg), however the degree was more extensive in cases of LPS-induced fever. Pretreatment of rabbits with reserpine (1 mg/kg, i.v.) suppressed the fever induced by an intravenous administration of LPS(0.5 microgram/kg), but did not suppress the release of endogenous pyrogen. These data suggest that endogenous pyrogen may not be an important factor in the pathogenesis of endotoxin fever.

摘要

静脉注射细菌内毒素(LPS)给兔子后,网状内皮系统(RES)释放内源性致热原可介导发热,这一点已有充分的文献记载。相反,通过消耗儿茶酚胺而具有多种药理活性的利血平会降低正常体温以及内毒素诱导的发热。在本文中,我们关注利血平对内源性致热原产生的影响及其与内毒素热解热作用的关系,得到以下结果:发热期间静脉注射LPS(0.5微克/千克)可检测到内源性致热原。然而,脑池内注射LPS(0.01微克/只)引发持久发热时,未检测到内源性致热原。利血平(1毫克/千克,静脉注射)可降低脑池内注射LPS(0.01微克/只)或静脉注射LPS(0.5微克/千克)所诱导的体温,但在LPS诱导发热的情况下降低程度更显著。用利血平(1毫克/千克,静脉注射)预处理兔子可抑制静脉注射LPS(0.5微克/千克)所诱导的发热,但不抑制内源性致热原的释放。这些数据表明内源性致热原可能不是内毒素热发病机制中的重要因素。

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