体外反搏对冠心病血小板聚集,TXB_2和6-酮-PGF_(1α)的影响

体外反搏(ECP)治疗16例冠心病人,其中11例测定了治疗前,治疗中1小时,1.5小时,2小时和停机后1小时,2小时以及一疗程后第二天清晨的血小板聚集,13例测定了治疗前,治疗中和一疗程结束时TXB_2和6-酮-PGF_(1a)。发现治疗2小时及以后各时段的血小板聚集率,TXB_2与治疗前比较有明显下降(P<0.01,P<0.05各自),6-酮PGF_(1a)明显升高(P<0.05)。本文指出,血流动力学的改变可影响血小板聚集,但主要是ECP治疗改善了微循环和组织代谢,保护了血管内皮使PGI_2合成增多,从而抑制了血栓的形成和冠状动脉痉挛,扩张了冠状动脉,此可能是ECP治疗冠心病的作用机制之一,并且在治疗心绞痛病人中防止了冠状动脉的进一步受损。

ECPS Effect to the PAG TXB_2,6-keto-PGF_(1α) of CHD

16 cases of potients with coronary artery disease had been treated be external counterpulsation(ECP). 11 cases had their platelet aggregation detced in pre--ECP, 1, 1 1/2 and 2 hours after the begining and 1, 2 hours after stopping of ECP, It was also estimated in the naxt morning after the whole course of ECP. We hed found that the patient's platelet aggregation and TXB_2 was decrcased since two hours after the begining(p<0.01, P<0.05 respectively). Besides, 6--keto--PGF_(1α) were increased(P<0.05) compared with that of pre--ECP.It seems that the change of circulatory dynamic can influence plateiet aggreation. It was possible that by improving the microcirculation and tissuse metabolism, ECP might protect the endothelium and thus accomodate syntheses of TXB_2 and PGI_2. It may be one of mechanism of efficacy of ECP and may thus prevent the injuring of coronary artery in thetrcatment of patient with angina pectoris.