Ferrara N, Abete P, Leosco D, Caccese P, Orlando M, Landino P, Sederino S, Tedeschi C, Rengo F
Istituto di Medicina Interna, Cardiologia e Chirurgia Cardiovascolare, II Facoltà di Medicina e Chirurgia, Napoli, Italy.
Arch Int Pharmacodyn Ther. 1990 Nov-Dec;308:104-14.
Flecainide acetate is a new antiarrhythmic drug which suppresses different kinds of experimental arrhythmias. We studied the efficacy of flecainide acetate on reperfusion- and barium-induced ventricular tachyarrhythmias in the isolated perfused rat heart by monitoring heart rate, coronary flow rate, left ventricular systolic pressure, dp/dtmax, and the voltage of the epicardial electrogram. Seventy-five male rats were randomized into 5 groups. In group I, after a 15 min period of stabilization, hearts were perfused by ischemic perfusion and then reperfused. In group II, flecainide acetate (10(-6) M) was given after stabilization and before ischaemic perfusion. In group III, barium chloride (10(-3) M) was given after stabilization. In group IV, flecainide acetate was given after stabilization and before barium chloride administration. In group V, acetylcholine chloride (10(-6) M) was given after stabilization and before barium chloride administration. In group I, we noted during ischemia a reduction in heart rate, coronary flow rate, left ventricular systolic pressure and dp/dtmax and an increase in the voltage of the epicardial electrogram. In group II, after administration of flecainide acetate, we observed a reduction in heart rate, left ventricular systolic pressure and dp/dtmax; during the ischaemic period there was no difference in these parameters with respect to group I. Reperfusion induced ventricular arrhythmias in 12 out of 15 hearts in group I and in only 3 out of 15 in group II (p less than 0.005). Barium induced ventricular arrhythmias in the 15 hearts studied in group III as well as in group IV. On the contrary, acetylcholine chloride in group V prevented the occurrence of barium-induced ventricular arrhythmias (p less than 0.005 vs group III and IV). Thus, flecainide acetate is able to reduce reperfusion-induced ventricular arrhythmias, but is unable to reduce barium-induced ventricular arrhythmias, presumably because of a different mechanism of these two types of arrhythmias.
醋酸氟卡尼是一种新型抗心律失常药物，可抑制多种实验性心律失常。我们通过监测心率、冠状动脉血流量、左心室收缩压、dp/dtmax以及心外膜电图电压，研究了醋酸氟卡尼对离体灌注大鼠心脏中再灌注和钡诱导的室性心律失常的疗效。75只雄性大鼠被随机分为5组。在第一组中，稳定15分钟后，心脏先进行缺血灌注然后再灌注。在第二组中，在稳定后且缺血灌注前给予醋酸氟卡尼（10(-6)M）。在第三组中，稳定后给予氯化钡（10(-3)M）。在第四组中，稳定后且在给予氯化钡之前给予醋酸氟卡尼。在第五组中，稳定后且在给予氯化钡之前给予氯化乙酰胆碱（10(-6)M）。在第一组中，我们注意到在缺血期间心率、冠状动脉血流量、左心室收缩压和dp/dtmax降低，心外膜电图电压升高。在第二组中，给予醋酸氟卡尼后，我们观察到心率、左心室收缩压和dp/dtmax降低；在缺血期，这些参数与第一组相比无差异。再灌注在第一组15只心脏中的12只诱发了室性心律失常，而在第二组15只中仅3只诱发了室性心律失常（p小于0.005）。钡在第三组和第四组研究的15只心脏中诱发了室性心律失常。相反，第五组中的氯化乙酰胆碱阻止了钡诱导的室性心律失常的发生（与第三组和第四组相比，p小于0.005）。因此，醋酸氟卡尼能够减少再灌注诱导的室性心律失常，但不能减少钡诱导的室性心律失常，推测是由于这两种类型心律失常的机制不同。
