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糖皮质激素对小鼠血小板活化因子-乙醚毒性的保护作用。

Glucocorticoid protection against PAF-acether toxicity in mice.

作者信息

Myers A, Ramey E, Ramwell P

出版信息

Br J Pharmacol. 1983 Jun;79(2):595-8. doi: 10.1111/j.1476-5381.1983.tb11034.x.

Abstract

Intravenous platelet activating factor (PAF-acether, 10 to 25 micrograms/kg body weight) produced dose-dependent mortality in both male and female mice. Pretreatment with indomethacin (50 mg/kg), verapamil (40 mg/kg) or nifedipine (4 mg/kg) failed to inhibit the lethal effect of 20 micrograms/kg PAF-acether. This suggests that neither arachidonate cyclo-oxygenase products nor availability of extracellular Ca2+ mediate the toxic action. In contrast, pretreatment with 100 mg/kg cortisone acetate (s.c.) daily for four days exerted a highly protective effect, i.e. 100% and 93% survival in males and females, compared to 13% and 7% respectively, in untreated animals. PAF-acether-induced death may be a useful model for the in vivo evaluation of pharmacological agents in anaphylactic shock.

摘要

静脉注射血小板活化因子(PAF-乙醚,10至25微克/千克体重)在雄性和雌性小鼠中均产生剂量依赖性死亡率。用吲哚美辛(50毫克/千克)、维拉帕米(40毫克/千克)或硝苯地平(4毫克/千克)预处理未能抑制20微克/千克PAF-乙醚的致死作用。这表明花生四烯酸环氧化酶产物和细胞外Ca2+的可用性均不介导毒性作用。相比之下,连续四天每天皮下注射100毫克/千克醋酸可的松预处理具有高度保护作用,即雄性和雌性的存活率分别为100%和93%,而未处理动物的存活率分别为13%和7%。PAF-乙醚诱导的死亡可能是体内评估过敏休克中药理剂的有用模型。

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