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目的研究β-受体阻滞剂阿替洛尔(atenolol)对急性心肌缺血后心室复极空间离散度的影响。方法本实验于1998—2002在Charles Sturt University医学院心血管病研究室完成。20只绵羊随机分成对照组和阿替洛尔组。结扎左冠状动脉的钝缘支诱导急性心肌缺血,同时在缺血区和非缺血区的64个心外膜位点描记单极心电图,从心外膜心电图上测量激动-恢复间期(activation-recovery intervals,ARI),最长和最短的ARI的差值定义为ARI离散度。结果阿替洛尔组缺血面积小于对照组[(13±2)%比(19±3)%,P<0.05];对照组ARI离散度在冠状动脉结扎后30、60和90min分别增加(18±21)、(27±21)和(16±10)ms(P<0.01),而在阿替洛尔组ARI的离散度无显著增加。结论阿替洛尔可抑制羊缺血诱导的心室复极空间离散度的增加。
Objective To study the effect of β-blocker atenolol on ventricular repolarization dispersion after acute myocardial ischemia. Methods This experiment was performed at the Charles Sturt University School of Medicine’s Cardiovascular Research Laboratory from 1998-2002. Twenty sheep were randomly divided into control group and atenolol group. Ligation of the blunt marginal branches of the left coronary artery induces acute myocardial ischemia, while monopolar electrocardiograms are recorded at 64 epicardial sites in the ischemic and non-ischemic areas and excitatory-recovery intervals ( activation-recovery intervals (ARI), the difference between the longest and shortest ARI is defined as the ARI dispersion. Results The ischemic area of atenolol group was smaller than that of control group [(13 ± 2)% vs (19 ± 3)%, P <0.05]; ARI dispersion of control group increased at 30, 60 and 90 minutes after coronary artery occlusion 18 ± 21), (27 ± 21) and (16 ± 10) ms, respectively (P <0.01), while there was no significant increase in ARI dispersion in the atenolol group. Conclusion Atenolol inhibits the increase of ventricular repolarization dispersion induced by sheep ischemia.