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将地塞米松注入兔终板血管器可通过原位抑制一氧化氮途径诱导解热。

Dexamethasone administered into organum vasculosum laminae terminalis of rabbits induced antipyresis via inhibiting nitric oxide pathway in situ.

作者信息

Lin M T, Lin J H, Yang Y L

机构信息

Department of Physiology, National Yang-Ming University, Taipei, Taiwan.

出版信息

Neurosci Lett. 1997 Jul 11;230(1):53-6. doi: 10.1016/s0304-3940(97)00463-1.

Abstract

Direct administration of lipopolysaccharide (LPS) into the organum vasculosum laminae terminalis (OVLT) increased the amount of nitric oxide (NO) release and inducible NO synthase expression. These increases paralleled the increase in deep body temperature in unanesthetized rabbits. Pretreatment with dexamethasone, a synthetic glucocorticoid, not only reduced the fever but also attenuated the NO release and the inducible NO synthase expression in the OVLT following an intra-OVLT dose of LPS. The data suggest that steroids such as dexamethasone exert their antipyresis by inhibiting the NO pathway in the OVLT of rabbit brain.

摘要

将脂多糖(LPS)直接注入终板血管器(OVLT)可增加一氧化氮(NO)释放量及诱导型一氧化氮合酶的表达。这些增加与未麻醉兔子深部体温的升高相一致。用合成糖皮质激素地塞米松预处理,不仅降低了发热,还减弱了在OVLT内注射一剂LPS后OVLT中的NO释放及诱导型一氧化氮合酶的表达。数据表明,地塞米松等类固醇通过抑制兔脑OVLT中的NO途径发挥其解热作用。

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