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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)。
In the guinea pig trachea and pulmonary artery rings, platelet activating factor (PAF) was found to not be able to constrict tracheal strips. In the presence of PAF, the histaminergic tracheal strips (105.6 ± 62.8%) were weaker than those without PAF (147.2 ± 71.8%), P <0.05. PAF and platelet suspension after suspension can cause tracheal contraction (24.5 ± 3.5%), diethylcarbamazine can reduce this contraction (14.5 ± 1.8%), P <0.05; indomethans have an increasing trend (31.1 ± 3.8% ). PAF can constrict the pulmonary artery rings, platelet presence, the deflation intensity (40.6 ± 5.4%) compared with no platelet (16.0 ± 2.9%) increased (P <0.01).