血栓素A2和血小板活化因子在豚鼠气道体内过敏性支气管收缩中的作用。

Role of thromboxane A2 and platelet-activating factor in allergic bronchoconstriction in guinea pig airway in vivo.

作者信息

Saito M, Fujimura M, Ogawa H, Matsuda T

机构信息

Third Department of Internal Medicine, Kanazawa University School of Medicine, Japan.

出版信息

J Lipid Mediat Cell Signal. 1995 Jan;11(1):1-12. doi: 10.1016/0929-7855(94)00023-6.

DOI:10.1016/0929-7855(94)00023-6

PMID:7728413

Abstract

Membrane-derived lipid mediators have been considered to play a major role in pathogenesis of bronchial asthma. However, the importance of and the interactions among each mediator are still unclear. We examined the role of thromboxane A2 (TXA2) and platelet-activating factor (PAF) in immediate asthmatic response (IAR) and interactions between these lipid mediators in guinea pig airway in vivo using a specific TXA2 antagonist S-1452 and a specific PAF antagonist Y-24180. We confirmed the activity of each antagonist, as S-1452 and Y-24180 significantly and dose-dependently inhibited bronchoconstriction induced by respective agonist inhalation. S-1452 inhibited IAR but Y-24180 did not, indicating that TXA2 plays a major role in IAR but PAF does not. S-1452 significantly inhibited PAF-induced bronchoconstriction but Y-24180 did not inhibit synthesized TXA2 (STA2)-induced bronchoconstriction, showing that the bronchoconstrictive effect of PAF is at least in part dependent on secondarily released TXA2, but TXA2 does not induce PAF production.

摘要

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。然而，每种介质的重要性及其相互作用仍不清楚。我们使用特异性血栓素A2（TXA2）拮抗剂S-1452和特异性血小板活化因子（PAF）拮抗剂Y-24180，研究了TXA2和PAF在豚鼠气道体内速发型哮喘反应（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S-1452和Y-24180显著且剂量依赖性地抑制了由各自激动剂吸入诱导的支气管收缩。S-1452抑制IAR，但Y-24180没有，这表明TXA2在IAR中起主要作用，而PAF不起主要作用。S-1452显著抑制PAF诱导的支气管收缩，但Y-24180不抑制合成血栓素A2（STA2）诱导的支气管收缩，表明PAF的支气管收缩作用至少部分依赖于继发性释放的TXA2，但TXA2不诱导PAF产生。