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一氧化氮合成的抑制可减轻大鼠体内细菌脂多糖诱导的低血压。

Inhibition of nitric oxide synthesis reduces the hypotension induced by bacterial lipopolysaccharides in the rat in vivo.

作者信息

Thiemermann C, Vane J

机构信息

William Harvey Research Institute, St Bartholomew's Hospital Medical College, London, U.K.

出版信息

Eur J Pharmacol. 1990 Jul 17;182(3):591-5. doi: 10.1016/0014-2999(90)90062-b.

DOI:10.1016/0014-2999(90)90062-b
PMID:2226626
Abstract

E. coli lipopolysaccharide (LPS; 15 mg kg-1 i.v.) produced a long-lasting reduction in mean arterial blood pressure (MAP) in the anaesthetized rat. Inhibition of nitric oxide endothelium-derived relaxing factor (EDRF) synthesis with NG-monomethyl-L-arginine (MeArg, 1 mg kg-1 min-1 i.v. for 30 min) produced an increase in MAP and largely attenuated the LPS-induced hypotension; both effects were significantly reversed with L-arginine (6 mg kg-1 min-1 i.v.). When compared to MeArg, phenylephrine (300 mg kg-1 h-1 i.v.) produced a similar pressor response, but much less attenuation of the hypotensive response to LPS. Thus, a stimulation of EDRF release contributes to the LPS-induced hypotension in the anaesthetized rat.

摘要

大肠杆菌脂多糖(LPS;15毫克/千克静脉注射)可使麻醉大鼠的平均动脉血压(MAP)出现持久下降。用N-甲基-L-精氨酸(MeArg,1毫克/千克·分钟静脉注射30分钟)抑制一氧化氮内皮源性舒张因子(EDRF)合成,可使MAP升高,并在很大程度上减弱LPS诱导的低血压;L-精氨酸(6毫克/千克·分钟静脉注射)可使这两种效应显著逆转。与MeArg相比,去氧肾上腺素(300毫克/千克·小时静脉注射)产生了类似的升压反应,但对LPS诱导的低血压反应的减弱作用要小得多。因此,EDRF释放的刺激作用促成了麻醉大鼠中LPS诱导的低血压。

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