Wainwright C L, Parratt J R, Bigaud M
Department of Physiology and Pharmacology, University of Strathclyde, Glasgow, Scotland.
Biomed Biochim Acta. 1988;47(10-11):S224-7.
These studies were performed to investigate a role of PAF in the genesis of life-threatening arrhythmias and platelet aggregation accompanying myocardial ischaemia and reperfusion. Pretreatment with the PAF antagonists SRI 63-441 (10 mgkg-1 iv) and BN 52021 (5 mgkg-1 iv) significantly reduced the number of arrhythmias during a thirty minute coronary artery occlusion period in open-chest anaesthetised greyhounds, particularly ventricular tachycardia. Both drugs also reduce the incidence of ventricular fibrillation resulting from reperfusion of the myocardium. Myocardial ischaemia in control animals resulted in a marked fall in platelet count in blood draining the ischaemic area, which was abolished by both SRI 63-441 and BN 52021. These results suggest a role for PAF in the genesis of ischaemia and reperfusion-induced arrhythmias, possibly by inducing platelet aggregation.
进行这些研究是为了探讨血小板活化因子(PAF)在伴随心肌缺血和再灌注出现的危及生命的心律失常及血小板聚集发生过程中的作用。用PAF拮抗剂SRI 63 - 441(10毫克/千克静脉注射)和BN 52021(5毫克/千克静脉注射)进行预处理,可显著减少开胸麻醉灵缇犬冠状动脉闭塞30分钟期间的心律失常数量,尤其是室性心动过速。两种药物还降低了心肌再灌注导致的心室颤动发生率。对照动物的心肌缺血导致缺血区域引流血液中的血小板计数显著下降,而SRI 63 - 441和BN 52021均可消除这种下降。这些结果表明PAF在缺血和再灌注诱导的心律失常发生过程中起作用,可能是通过诱导血小板聚集。