PAF受体拮抗剂对缺氧性肺血管收缩和PAF舒血管反应的影响

Effects of PAF Receptor Antagonists on Pulmonary Hypoxic Vasodilation and PAF-Induced-Vasodilation in Rats

用SRI63-441和BN52021两种结构不同的血小板活化因子(PAF)受体拮抗剂,研究其对整体大鼠缺氧性肺血管收缩反应(HPV)的影响及对PAF舒血管反应的抑制作用。结果两种PAF受体拮抗剂均可抑制由PAF诱导的舒血管反应,并增加基础状态下肺动脉压、肺血管阻力,但对HPV无明显影响。提示PAF的舒血管反应通过受体起作用,内源性PAF在维持肺动脉低张状态中可能起一定的作用,而在HPV中不起主要作用。

We studied the effects of two structurally dissimilar PAF receptor antagonists, SRI63-441 and BN52021, on pulmonary hypoxic vasoconstriction (HPV) and PAF-induced-vasodilation in rats. Owr experimental results show that both SRI63-441 and BN52021 block the vasodilation induced by PAF and increase mean pulmonary artery pressure and pulmonary vascular resistance of baseline, without exerting any effects on HPV. The present study suggests that endogenous PAF may play a certain role in. maintaining low pulmonary vascular tone, but not a major role in HPV. It is also suggested that the vasodilation induced by PAF may be mediated by the receptor.