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先前的研究表明血小板α_2受体变化表征交感神经突触前α_2受体的变化。为了解心衰病人血小板α_2受体功能状况,我们观察了10例Ⅲ、Ⅳ级心功能的心衰病人及10例配对正常人由肾上腺素诱导的血小板聚集率在α_2受体阻滞前后的变化。结果表明肾上腺素诱导的血小板聚集率在两组无显著性差异,但应用α_2阻滞剂Rauwolscine(0.25mg/L)后,0.25,0.5,1.0mg/L E诱导的心衰病人血小板聚集率显著低于对照组,提示血小板α_2受体在心衰时有数量的减少或(和)功能的降低,表征交感神经突触前NE释放的负反馈机制被抑制。
Previous studies have shown that changes in platelet alpha 2 receptors characterize sympathetic presynaptic alpha 2 receptor changes. To understand the function of platelet α_2 receptor in patients with heart failure, we observed changes of platelet aggregation induced by adrenaline before and after α_2 receptor block in 10 patients with heart failure of grade Ⅲ and Ⅳ and 10 matched normal subjects . The results showed that there was no significant difference in the rate of platelet aggregation induced by epinephrine between the two groups, but the platelet aggregation rate was significantly lower in patients with heart failure induced by 0.25,0.5,1.0 mg / LE after the α 2 blocker Rauwolscine (0.25 mg / L) In the control group, it was suggested that there was a decrease in the number of (or) platelet alpha 2 receptors in heart failure and a negative feedback mechanism characterizing the NE release before sympathetic synapse was inhibited.