Vasilets L A, Mokh V P
Biull Eksp Biol Med. 1987 May;103(5):593-5.
An antiarrhythmic action of water-soluble antioxidant SD-6 from 3-hydroxypyridine class and its effect on the transmembrane potentials were studied using the isolated rat heart and papillary muscle. Ischemia was induced by the occlusion of the left anterior descending coronary artery. 10 minutes later the ligation was removed and reperfusion was achieved. In the control, ischemia induced premature ventricular complexes, tachycardia and, in some cases, fibrillation. During perfusion total fibrillation occurred in 100% of the experiments. SD-6 in the doses of 10(-6) g/ml and 5 X 10(-6) g/ml significantly reduced the incidence of fibrillation and tachycardia. In the experiments on the papillary muscle SD-6 during reperfusion completely normalized the action potential duration and removed depolarization developed in hypoxia, which suggests the ability of the antioxidant to block reperfusion-induced arrhythmias by normalization of the parameters of electrical heterogeneity. These data show that the origin of reperfusion-induced arrhythmias is connected with the activation of free radical metabolites and that their scavengers--synthetic antioxidants from 3-hydroxypyridine class--can be used as new antiarrhythmic agents.
利用离体大鼠心脏和乳头肌，研究了3-羟基吡啶类水溶性抗氧化剂SD-6的抗心律失常作用及其对跨膜电位的影响。通过结扎左冠状动脉前降支诱导心肌缺血。10分钟后松开结扎线实现再灌注。在对照组中，缺血诱发室性早搏、心动过速，在某些情况下还诱发颤动。在灌注过程中，100%的实验发生了完全性颤动。剂量为10(-6) g/ml和5×10(-6) g/ml的SD-6显著降低了颤动和心动过速的发生率。在乳头肌实验中，再灌注期间的SD-6使动作电位时程完全恢复正常，并消除了缺氧时出现的去极化，这表明抗氧化剂能够通过使电不均一性参数正常化来阻断再灌注诱发的心律失常。这些数据表明，再灌注诱发心律失常的起源与自由基代谢产物的激活有关，而它们的清除剂——3-羟基吡啶类合成抗氧化剂——可用作新型抗心律失常药物。
