血小板活化因子与血小板对离体豚鼠气管和肺动脉平滑肌的影响

Effects of Platelet-activating Factor and Platelets on the Isolated Tracheal and Pulmonary Arterial Smooth Muscles of Guinea Pig

以离休豚鼠气管条和肺动脉环实验发现血小板活化因子(PAF)不能收缩气管条,PAF存在时,组织胺收缩气管条强度(105.6±62.8％)较无PAF时(147.2±71.8％)弱,P<0.05。PAF与血小板共孵后悬液可致气管条收缩(24.5±3.5％),乙胺嗪可减弱这种收缩(14.5±1.8％),P<0.05;消炎痛则有增强趋势(31.1±3.8％)。PAF能收缩肺动脉环,血小板存在时,缩管强度(40.6±5.4％)较无血小板时(16.0±2.9％)有所增强(P<0.01)。

On the isolated tracheal strips and pulmonary arterial rings of guinea pig we tested the effects of platelet-activating factor(PAF) and platelets on airway and pulmonary vascular smooth muscles. It was found that PAF could not induce the contraction of tracheal strips. In the presence of PAF, the strength of contraction of the tracheal strips induced by histamine was 105.6 ± 62.8%, which was lower than thatinthe absence of PAF (147.2 ± 71.8%, n=5,P<0.05). When co-incubated with PAF for 20 min, platelet suspension could cause the contraction of tracheal strips, the strength of which was 24.5 ±3.5% (n=6). This constriction was partially inhibited by diethylcarbamazine (14.5 ±1.8%, n=5, P<0.05) and may be slightly enhanced by indomethacine (31.1 ±3.8%, n=4, P>0.05). PAF had a direct constrictive effect on pulmonary rings (16.0 ±2.9%, n=5), which could be further amplified in the presence of platelets (40.6±5.4%,n=6, P<0.01). From the above we may speculate that PAF and platelets play a role in the development of asthma and pulmonary hypertension.