摘要
目的:研究氧苦参碱对心肌梗死犬心律失常的作用。方法:部分结扎犬左冠状动脉前降支,造成前壁心肌梗死,5—8d后,使用程控电刺激技术(PES),测定心肌舒张期兴奋阈值(DET)和有效不应期(ERP),并诱发心律失常,然后造成冠状动脉左旋支急性栓塞,观察室颤发生。结果:Oxy(iv50mg·kg^(-1))明显提高DET(由2.53±1.28至3.19±1.62V),延长左室正常区ERP(由182±25至219±43ms)及梗塞区ERP(由206±49至235±55ms),但对ERP离散性,QTc间期及VT/VF无影响;Pro(iv25mg·kg^(-1))则能提高DET,延长ERP及QTc间期,缩小ERP离散性,预防PES诱发的VT/VF及再缺血所致VF。结论:Oxy提高DET,延长ERP是其抗心律失常的机制。
AIM: TO study the effects of oxymatrine (Oxy) on arrhythmia in dogs with myocardial infarction. METHODS: Partly ligating the left anterior descending coronary artery in the open-chest dogs produced myocardial infarction of left anterior ventricular wall. After 5 - 8 d, the diastolic excitability threshold ( DET ), the effective refractory periods (ERP) and arrhythmias were determined by programmed electric stimulation (PES). RESULTS: Oxy (iv 50 mg·kg-1) increased DET from 2.53 ± 1.28 to 3.19 ± 1.62 V, lengthened ERP from 182 ± 25 to 219 ± 43 ms at normal region and from 206 ± 49 to 235 ± 55 ms at infarct region in left ventricle, but had no effects on dispersion of ERP, QTc interval and ventricular tachycardia (VT) or ventricular fibrillation (VF). Procainarnide (Pro) (iv 25 mg·kg-1) increased DET and lengthened ERP and QTc interval, but decreased the dispersion of ERP. Pro prevented PES-induced VT/VF and spontaneous ischemia-related VF. CONCLUSION: The increased DET and lengthened ERP of Oxy are its anti-arrhythmic mechanism.
出处
《中国药理学报》
CSCD
1996年第4期379-382,共4页
Acta Pharmacologica Sinica
关键词
氧苦参碱
心肌梗死
心律失常
oxymatrine
myocardial infarction
arrhythmia