Kusama Y, Hearse D J, Avkiran M
Cardiovascular Research, Rayne Institute, St. Thomas' Hospital, London, UK.
J Mol Cell Cardiol. 1992 Apr;24(4):411-21. doi: 10.1016/0022-2828(92)93195-p.
Studies using chemically-induced models of diabetes have shown the diabetic myocardium to exhibit abnormalities in cellular ion transport, which may affect susceptibility to reperfusion-induced arrhythmias. We studied the incidence of reperfusion-induced ventricular tachycardia (VT) and fibrillation (VF) in isolated hearts from rats with streptozotocin-induced diabetes and from age-matched and weight-matched control rats (n = 12 per group). Following 5 min of regional ischaemia, reperfusion resulted in a similarly low incidence of arrhythmias in all three groups. Following 10 min of regional ischaemia, the incidence of VT was 92, 100 and 92%, and the incidence of VF was 75, 92 and 92% in diabetic, age-matched control and weight-matched control groups, respectively (NS). However, among those hearts which exhibited VF, the incidence of sustained (greater than or equal to 120 s) VF was 73 and 55% in age-matched and weight-matched control groups, respectively, and 0% in the diabetic group (P less than 0.05 vs both controls). The mean duration of VF in the diabetic group was reduced from 201 +/- 33 and 171 +/- 36 s in age-matched and weight-matched control groups, respectively, to 9 +/- 3 s (P less than 0.05). Thus, streptozotocin-induced diabetes in the rat does not result in an increased susceptibility to reperfusion-induced arrhythmias. To the contrary, hearts from diabetic rats are less susceptible to potentially lethal arrhythmias during reperfusion. Likely contributory factors to this phenomenon include (i) increased myocardial content of free radical scavenging enzymes, (ii) prolonged action potential duration, and (iii) reduced activity of sarcolemmal Na+/H+ and Na+/Ca2+ exchange processes, all of which have previously been reported in similar models of diabetes.
使用化学诱导糖尿病模型的研究表明，糖尿病心肌在细胞离子转运方面存在异常，这可能会影响对再灌注诱导心律失常的易感性。我们研究了链脲佐菌素诱导糖尿病大鼠以及年龄匹配和体重匹配的对照大鼠（每组n = 12）离体心脏中再灌注诱导的室性心动过速（VT）和颤动（VF）的发生率。局部缺血5分钟后，再灌注导致三组的心律失常发生率同样较低。局部缺血10分钟后，糖尿病组、年龄匹配对照组和体重匹配对照组的VT发生率分别为92%、100%和92%，VF发生率分别为75%、92%和92%（无显著性差异）。然而，在那些出现VF的心脏中，年龄匹配和体重匹配对照组的持续性（大于或等于120秒）VF发生率分别为73%和55%，而糖尿病组为0%（与两个对照组相比，P < 0.05）。糖尿病组VF的平均持续时间从年龄匹配对照组的201±33秒和体重匹配对照组的171±36秒分别降至9±3秒（P < 0.05）。因此，链脲佐菌素诱导的大鼠糖尿病不会导致对再灌注诱导心律失常的易感性增加。相反，糖尿病大鼠的心脏在再灌注期间对潜在致命性心律失常的易感性较低。导致这种现象的可能因素包括：（i）心肌自由基清除酶含量增加；（ii）动作电位持续时间延长；（iii）肌膜Na+/H+和Na+/Ca2+交换过程活性降低，所有这些在类似的糖尿病模型中此前均有报道。
