Saito M, Fujimura M, Ogawa H, Matsuda T
Third Department of Internal Medicine, Kanazawa-University School of Medicine, Japan.
Prostaglandins Leukot Essent Fatty Acids. 1993 Aug;49(2):579-85. doi: 10.1016/0952-3278(93)90164-r.
Membrane-derived lipid mediators have been considered to play a major role in pathogenesis of bronchial asthma. Recently specific antagonists and synthetase inhibitors of some chemical mediators have been developed and many studies on their anti-asthmatic effects are ongoing. But the importance of and the interactions of each mediator are still unclear. We examined the role of leukotrienes (LTs) and platelet activating factor (PAF) in immediate asthmatic response (IAR) and interactions between these lipid mediators in guinea pig airways in vivo using a specific LTs antagonist AS-35 and a specific PAF antagonist Y-24180. We confirmed the activity of each antagonist, as AS-35 and Y-24180 inhibited bronchoconstriction induced by respective agonist inhalation. AS-35 inhibition IAR but Y-24180 did not, indicating that LTs play a major role in IAR but PAF does not. AS-35 did not influence PAF-induced bronchoconstriction and Y-24180 did not inhibit LTs-induced bronchoconstriction, showing that there is no interaction between LTs and PAF.
膜衍生脂质介质被认为在支气管哮喘的发病机制中起主要作用。最近，一些化学介质的特异性拮抗剂和合成酶抑制剂已被开发出来，并且关于它们抗哮喘作用的许多研究正在进行。但是每种介质的重要性及其相互作用仍不清楚。我们使用特异性白三烯（LTs）拮抗剂AS - 35和特异性血小板活化因子（PAF）拮抗剂Y - 24180，在豚鼠气道体内研究了白三烯（LTs）和血小板活化因子（PAF）在速发型哮喘反应（IAR）中的作用以及这些脂质介质之间的相互作用。我们证实了每种拮抗剂的活性，因为AS - 35和Y - 24180抑制了各自激动剂吸入诱导的支气管收缩。AS - 35抑制IAR，但Y - 24180没有，表明白三烯在IAR中起主要作用，而血小板活化因子不起主要作用。AS - 35不影响PAF诱导的支气管收缩，Y - 24180不抑制白三烯诱导的支气管收缩，表明白三烯和血小板活化因子之间没有相互作用。
