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作 者:钟江华[1] 陈小盼[1] 姚震[1] 杨新玮[1]
出 处:《实用药物与临床》2008年第6期336-338,共3页Practical Pharmacy and Clinical Remedies
基 金:海南省教育厅科研基金项目(Hj200306)
摘 要:目的研究比索洛尔对慢性充血性心力衰竭(CHF)中层心肌复极异质性的影响。方法制作CHF家兔模型,并给予比索洛尔干预,然后分别测定其室颤阈值(VFT)以及心外膜、中层心肌和心内膜心肌细胞的单相动作电位复极90时程(APD90)、跨室壁复极离散度(TDR)。结果CHF组3层心肌APD90均明显延长,但中层心肌APD90延长更为明显,跨室壁TDR增加,VFT明显降低。而与CHF组相比,比索洛尔治疗组(CHF+BIS),3层心肌APD90均进一步延长,以心内、外层心肌APD90延长更为明显,TDR减小,VFT阈值升高。结论比索洛尔能减小CHF3层心肌跨室壁复极不均一性,抑制恶性室性心律失常的发生。Objective To study the effects of Bisoprolol on midmyocardial repolarization in rabbit models with congestive heart failure(CHF). Methods Bisoprolol was used to treat the rabbit models of CHF, and evaluating ventricular fibrillation threshold(VFT), transmural dispersion of repolarization(TDR) and action potential duration at 90 % repolarization(APD) in epicardium, midmyocardium and endocardium. Results Compared with the control group, VFT remarkably decreased, and all APD of 3 myocardial layers were extended in rabbits with CHF, while the extension of midmyocardium was more markedly. TDR significantly increased in CHF. Treatment with Bisoprolol further extended APD of 3 myocardial layers in CHF rabbits, the extension was more marked in endoeardium and epicardium, and the TDR significantly decreased, VFT increased. Conclusion Bisoprolol can decrease the transmural heterogeneity of ventricular repolarization and depress malignant ventricular arrhythmias in CHF.
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