Bessin P
Pharmacol Res Commun. 1986 Aug;18 Suppl:139-50. doi: 10.1016/0031-6989(86)90047-0.
The fact that PAF-acether elicites acute circulatory collapse in anesthetized dogs supports the hypothesis that its endogenous double is involved in shock state events. The fact that cysteinyl containing leukotrienes has been shown to be released in various shock states, themselves producing noxious effects related to such circulatory disturbances, suggests a possible role of these arachidonic acid metabolites in shock syndrome. The present report summarizes the part played by these mediators in shock developments. More precisely, nanograms PAF-acether IV in anesthetized dogs produced biphasic effects on mesenteric blood flow and inhibited, in dogs and rats, histamine induced gastric acid secretion. These results confirm the distributive component of the PAF-acether circulatory collapse. On the other hand, as leukotrienes, nanograms PAF-acether elicited both plasma extravasation and vasoconstriction in guinea pig skin. Lastly, in conscious mice, lipoxygenase antagonists, but not cyclooxygenase antagonists, inhibited lethal effects of PAF-acether, suggesting a mutual and synergistic action of PAF-acether and leukotrienes in shock state.
血小板活化因子（PAF - 乙醚）能使麻醉犬发生急性循环衰竭，这一事实支持了以下假说：其内源性类似物参与了休克状态事件。含半胱氨酰白三烯已被证明在各种休克状态下会释放出来，它们自身会产生与这种循环紊乱相关的有害作用，这表明这些花生四烯酸代谢产物在休克综合征中可能发挥作用。本报告总结了这些介质在休克发展过程中所起的作用。更确切地说，给麻醉犬静脉注射纳克级的PAF - 乙醚会对肠系膜血流产生双相作用，并在犬和大鼠中抑制组胺诱导的胃酸分泌。这些结果证实了PAF - 乙醚循环衰竭的分布性成分。另一方面，与白三烯一样，纳克级的PAF - 乙醚在豚鼠皮肤中会引起血浆外渗和血管收缩。最后，在清醒小鼠中，脂氧合酶拮抗剂而非环氧化酶拮抗剂能抑制PAF - 乙醚的致死作用，这表明PAF - 乙醚与白三烯在休克状态下存在相互协同作用。
