Dresel P E, Ogbaghebriel A, Abraham R
Can J Physiol Pharmacol. 1985 Nov;63(11):1418-22. doi: 10.1139/y85-233.
His-bundle electrocardiography was used to evaluate the effects of ethmozine on cardiac conduction in isolated perfused rabbit hearts electrically driven at cycle lengths of 320 and 250 ms. There was no significant change in conduction until high concentrations of ethmozine were reached. His-Purkinje and atrioventricular (AV) nodal conduction were slowed significantly at 0.1 microgram/mL and atrial conduction at 1.0 microgram/mL. Conduction block occurred at 10.0 micrograms/mL in all the hearts treated. Effects of the drug (0.1 and 0.01 microgram/mL) on conduction of extrasystoles were also studied in hearts driven at a basic cycle length of 270 ms. No significant change was observed in atrial conduction of extrasystoles throughout the coupling intervals tested at both concentrations. Ethmozine (0.01 and 0.1 microgram/mL) caused slowing of His-Purkinje conduction of extrasystoles but the effect of the drug did not change as a function of the coupling interval. An interval-dependent increase in AV-nodal conduction time was observed, with the maximum slowing of conduction occurring at coupling intervals close to the effective refractory period of the AV node. AV-nodal functional refractory period was increased significantly by ethmozine (0.01 and 0.1 microgram/mL). The effective refractory period was significantly increased only at the higher concentration.
采用希氏束心电图技术,在320和250毫秒心动周期长度电驱动的离体灌注兔心脏中,评估乙吗噻嗪对心脏传导的影响。在达到高浓度乙吗噻嗪之前,传导无显著变化。在0.1微克/毫升时,希氏-浦肯野纤维和房室(AV)结传导显著减慢,在1.0微克/毫升时心房传导减慢。在所有接受治疗的心脏中,10.0微克/毫升时出现传导阻滞。还在基础心动周期长度为270毫秒驱动的心脏中研究了该药物(0.1和0.01微克/毫升)对期外收缩传导的影响。在两种浓度下测试的整个配对间期内,期外收缩的心房传导均未观察到显著变化。乙吗噻嗪(0.01和0.1微克/毫升)导致期外收缩的希氏-浦肯野纤维传导减慢,但药物的作用并不随配对间期而改变。观察到房室结传导时间呈间期依赖性增加,在接近房室结有效不应期的配对间期时传导减慢最大。乙吗噻嗪(0.01和0.1微克/毫升)显著增加了房室结功能不应期。仅在较高浓度时有效不应期显著增加。