Terashita Z, Imura Y, Nishikawa K, Sumida S
Eur J Pharmacol. 1985 Feb 26;109(2):257-61. doi: 10.1016/0014-2999(85)90427-3.
To determine whether endogenous PAF contributes to the pathogenesis of endotoxin shock, CV-3988, a specific PAF antagonist, was injected i.v. to rats before, simultaneously with or after endotoxin. CV-3988 (5 mg/kg i.v.) injected 5 min before the endotoxin completely inhibited endotoxin (15 mg/kg i.v.)-induced hypotension, and CV-3988 (0.05-1 mg/kg i.v.) injected 7-10 min after the endotoxin rapidly reversed endotoxin-induced hypotension. A combination of CV-3988 (10 mg/kg) with endotoxin (5 mg/kg) administered i.v. improved the survival rate for 20 h or more. CV-3988 (0.05-1 mg/kg i.v.) rapidly reversed the PAF (1 microgram/kg i.v.)-induced hypotension. These findings strongly suggest that endogenous PAF may play a pivotal role in the pathogenesis of endotoxin shock.
为了确定内源性血小板活化因子（PAF）是否参与内毒素休克的发病机制，在给大鼠静脉注射内毒素之前、同时或之后，静脉注射特异性PAF拮抗剂CV-3988。在内毒素注射前5分钟静脉注射CV-3988（5毫克/千克）可完全抑制内毒素（15毫克/千克静脉注射）诱导的低血压，在内毒素注射后7至10分钟静脉注射CV-3988（0.05至1毫克/千克）可迅速逆转内毒素诱导的低血压。静脉注射CV-3988（10毫克/千克）与内毒素（5毫克/千克）的组合可提高20小时或更长时间的存活率。CV-3988（0.05至1毫克/千克静脉注射）可迅速逆转PAF（1微克/千克静脉注射）诱导的低血压。这些发现强烈表明内源性PAF可能在内毒素休克的发病机制中起关键作用。
