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肺中血小板激活因子(PAF)介导反应的机制。

Mechanisms of platelet-activating factor (PAF)-mediated responses in the lung.

机构信息

Division Pulmonary Pharmacology, Research Center Borstel, Leibniz-Center for Medicine and Biosciences, Parkallee 22, 23845 Borstel, Germany.

出版信息

Pharmacol Rep. 2005;57 Suppl:206-21.

Abstract

Platelet-activating factor (PAF) is a potent lipid mediator that has been implicated in asthma, sepsis, acute lung injury and ischemia/reperfusion injury. Its actions in the lungs include vasoconstriction, bronchoconstriction, and edema formation. Despite the fact that PAF exerts these actions within minutes, they are mediated by other lipid mediators, in particular eicosanoids generated by cyclooxygenase and lipoxygenase enzymes and sphingolipids generated by acid sphingomyelinase.We will discuss the mechanisms of the PAF-induced pressor responses that are triggered by thromboxane A(2) and leukotrienes, as well the PAF-induced increase in vascular permeability that is mediated by prostaglandin E(2) (PGE(2)) and ceramide.

摘要

血小板激活因子(PAF)是一种强效的脂质介质,与哮喘、脓毒症、急性肺损伤和缺血/再灌注损伤有关。其在肺部的作用包括血管收缩、支气管收缩和水肿形成。尽管 PAF 在数分钟内发挥这些作用,但它们是由其他脂质介质介导的,特别是由环加氧酶和脂加氧酶产生的类二十烷酸和酸性鞘磷脂酶产生的鞘脂。我们将讨论由血栓烷 A2 和白三烯引发的 PAF 诱导的升压反应的机制,以及由前列腺素 E2(PGE2)和神经酰胺介导的 PAF 诱导的血管通透性增加。

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