Becker K, Förster W
Department of Pharmacology and Toxicology, Martin Luther University, Halle-Wittenberg, GDR.
Biomed Biochim Acta. 1988;47(10-11):S169-72.
The PAF-acether mortality in female mice varied with strains: AB mice were very resistant, NMRI mice showed dose-dependent effects. We used an i.v. injection of 75 micrograms/kg PAF-acether resulting in a 75% mortality in NMRI mice. Nileprost and PGE1 in one tenth of the doses of iloprost or PGI2 were able to reduce the PAF-acether mortality. Nalador, PGE2 and flunoprost were ineffective. 10 min after PAF application the TXB2 content in tail skin was increased significantly. The inhibitory effect on the TXB2 release induced by A 23187 from human granulocytes was stronger by nileprost than by iloprost. Nalador was ineffective, flunoprost enhanced the release. The lowered TXB2 formation is a possible explanation for the prevention of the PAF-acether induced death by PGs.
雌性小鼠中血小板活化因子(PAF)-乙醚的致死率因品系而异:AB小鼠具有很强的抗性,NMRI小鼠呈现剂量依赖性效应。我们通过静脉注射75微克/千克的PAF-乙醚,导致NMRI小鼠有75%的死亡率。尼罗前列素和前列腺素E1以伊洛前列素或前列环素(PGI2)十分之一的剂量能够降低PAF-乙醚的致死率。纳拉多、前列腺素E2和氟诺前列素无效。应用PAF后10分钟,尾部皮肤中血栓素B2(TXB2)的含量显著增加。尼罗前列素对A 23187诱导人粒细胞释放TXB2的抑制作用比伊洛前列素更强。纳拉多无效,氟诺前列素增强了释放。TXB2生成降低是PGs预防PAF-乙醚诱导死亡的一种可能解释。