Pacher P, Ungvári Z, Nánási P P, Kecskeméti V
Department of Pharmacology, Semmelweis University of Medicine, Budapest, Hungary.
Acta Physiol Scand. 1999 May;166(1):7-13. doi: 10.1046/j.1365-201x.1999.00538.x.
Action potential configuration in ventricular and atrial myocardium, as well as rate-dependent changes in ventricular action potential duration (APD) were studied and compared in healthy and diabetic rats. Diabetes was induced by a single injection of streptozotocin (STZ, 65 mg kg(-1) i.v.). Conventional microelectrode techniques were applied to record action potentials after the establishment of diabetes (2, 6, 10 and 18 weeks after STZ-treatment). Untreated age-matched animals were used as controls. Both depolarization and repolarization were significantly retarded following STZ-treatment. However, the time course of development of diabetic changes in atrial and ventricular myocardium was different. APD was significantly lengthened from week 2 of diabetes in ventricular, but only from week 6 in atrial preparations. In atrial myocardium, lengthening of APD was more pronounced at early rather than late phases of repolarization. The maximum rate of depolarization (Vmax) was significantly reduced from the 6th week of diabetes in both preparations. No differences were observed in action potential amplitude (except at week 18) and in the resting membrane potential in diabetic rats. Diabetic ventricular preparations showed a positive APD-frequency relationship at any level of repolarization, in contrast to control muscles, where APD25 and APD50 values lengthened. But APD75 and APD90 values were not changed significantly with increase in the pacing frequency. The results indicate that development of diabetic alterations are not fully identical in atrial and ventricular myocardium of the rat, probably owing to differences in density and kinetics of ionic currents responsible for atrial and ventricular action potentials.
在健康大鼠和糖尿病大鼠中研究并比较了心室和心房心肌的动作电位形态，以及心室动作电位时程（APD）的频率依赖性变化。通过单次静脉注射链脲佐菌素（STZ，65 mg kg⁻¹）诱导糖尿病。在糖尿病建立后（STZ治疗后2、6、10和18周），应用传统微电极技术记录动作电位。将未治疗的年龄匹配动物用作对照。STZ治疗后，去极化和复极化均明显延迟。然而，心房和心室心肌糖尿病性变化的发展时间进程不同。糖尿病第2周时心室APD显著延长，但心房标本仅在第6周时APD才显著延长。在心房心肌中，APD延长在复极化早期比晚期更明显。两种标本中，糖尿病第6周起最大去极化速率（Vmax）显著降低。糖尿病大鼠的动作电位幅度（第18周除外）和静息膜电位未见差异。与对照肌肉相反，糖尿病心室标本在任何复极化水平均呈现APD-频率正相关，对照肌肉中APD25和APD50值延长，但APD75和APD90值随起搏频率增加未显著改变。结果表明，大鼠心房和心室心肌糖尿病性改变的发展并不完全相同，这可能是由于负责心房和心室动作电位的离子电流密度和动力学存在差异。
