血小板活化因子的支气管收缩作用及其机理研究

Platelet-activating factor induced bronchoconstriction and possible mechanisms

本文研究了血小板活化因子(PAF)对豚鼠在体和离体支气管平滑肌的收缩作用,同时对PAF的这一作用机制进行了讨论。结果:1.PAF静脉和雾化吸入均迅速引起支气管收缩,并伴有外周循环血小板数减少。2.单纯PAF对离体支气管平滑肌条的收缩作用微弱,当加入洗涤血小板后其收缩作用明显增强。3.血栓素A_2受体拮抗剂(AA-2414)明显抑制了PAF加血小板而引起的支气管平滑肌收缩。提示PAF对支气管平滑肌可有直接作用,但其通过血小板引起收缩作用更强;经PAF激活的血小板主要通过释放血栓素A_2参与支气管收缩。

The effect of platelet activating factor (PAF) on bronchial smooth muscleboth in vitro and in vivo in guinea-pigs were observed and its mechanism explored. Theresults showed: 1. Bronchoconstriction can be induced by PAF both by i. v. and via aerosoladministration and was accompanied with a fall of the circulating platelet count. 2. Thecontractile effect of PAF on guinea-pig airway smooth muscle preparations is modest invitro. Yet this effect of PAF can be enhanced by platelet. 3. TXA_2 receptor antagonist(AA-2414) can inhibit bronchoconstriction induced by PAF with platelet significantly.These results suggested that PAF might be a potent endogenous bronchoconstrictor and itseffect was related to platelet. The activated platelets can induce bronchoconstriction byreleasing TXA_2.