Effects of intravenous anesthetics on atrial wavelength and atrioventricular nodal conduction in guinea pig heart. Potential antidysrhythmic properties and clinical implications.
Effects of intravenous anesthetics on atrial wavelength and atrioventricular nodal conduction in guinea pig heart. Potential antidysrhythmic properties and clinical implications.
复制标题
静脉麻醉药对豚鼠心脏心房波长和房室结传导的影响。
DOI：
10.1097/00000542-199608000-00022
复制
发表时间：
1996
期刊：
影响因子：
8.8
通讯作者：
Dennis,DM
中科院分区：
文献类型：
--
作者：
Napolitano,CA;Raatikainen,MJ;Martens,JR;Dennis,DM
背景房颤等室上性心动过速常常使围手术期并发症增多。室上性心动过速发生的两个关键电生理因素是：1)房室传导速度(CV)和有效不应期(ERP)的乘积--心房波长；2)房室结传导。药物对这些因子的调节具有重要的临床意义。研究了异丙酚、硫喷妥钠和氯胺酮对豚鼠离体房小梁和心脏心房波长和房室结功能的影响。在单个房小梁上放置一个刺激电极和两个记录电极，测量电极间距离。心房事件相关电位的测定是使用提前刺激方案进行的。测量了传播脉冲穿过极间距离(D)所需的时间(T)。以d/t为单位计算传导速度。用Langendorff灌流的豚鼠心脏进行低度心房起搏(周期=300ms)，并测量刺激至希氏束间期间期房室结传导指数。为了研究房室结的频率依赖性行为，在计算机上测量了文克巴赫周期长度(WCL)和房室结ERP。结果硫柳汞以浓度依赖的方式显著延长房室结的ERP，而异丙酚和氯胺酮对心房不应期无明显影响。氯胺酮呈剂量依赖性降低房性心动过速，而异丙酚和硫喷妥钠对心房性心动过速无明显影响。因此，硫喷妥钠、氯胺酮和异丙酚分别引起心房波长的增加、减少和无变化。所有麻醉剂均引起刺激-希氏束间期、房室结ERP和WCL的浓度依赖性延长。然而，在等摩尔的基础上，发现了显著的效力差异。使异丙酚、硫喷妥钠和氯胺酮的ERP(ERP20)和WCL(WCL20)增加20%的药物浓度分别为14+/-2微米、26+/-3微米和62+/-11微米和17+/-2微米、50+/-1微米和123+/-19微米(平均+/-扫描电子显微镜)。因此，频率依赖性房室结效应的药效顺序为异丙酚>硫喷妥钠>氯胺酮。结论在室上性心动过速时，异丙酚对房性冲动的滤过率最高，而硫喷妥钠预防房折返性心律失常最有效。相反，氯胺酮可能最有可能促进心房折返，而对房室结传导的影响最小。
BackgroundSupraventricular tachydysrhythmias such as atrial fibrillation frequently complicate the perioperative period. Two electrophysiologic factors critical to the pathogenesis of supraventricular tachydysrhythmias are: 1) atrial wavelength, the product of atrial conduction velocity (CV) and effective refractory period (ERP), and 2) atrioventricular nodal conduction. Modulation of these factors by drugs has important clinical ramifications. The authors studied the effects of propofol, thiopental, and ketamine on atrial wavelength and atrioventricular nodal function in guinea pig isolated atrial trabeculae and hearts, respectively.MethodsElectrocardiogram recordings in superfused atrial tissue were obtained using hanging microelectrodes. A stimulating and two recording electrodes were placed on a single atrial trabecula, and the interelectrode distance was measured. Atrial ERP determinations were made using a premature stimulus protocol. The time (t) required for a propagated impulse to traverse the interelectrode distance (d) was measured. Conduction velocity was calculated as d/t. Langendorff-perfused guinea pig hearts were instrumented for low atrial pacing (cycle length= 300 ms) and for measurements of stimulusto-His bundle interval, an index of atrioventricular nodal conduction. To investigate the frequency-dependent behavior of the atrioventricular node, computer-based measurements were made of Wenckebach cycle length (WCL) and atrioventricular nodal ERP.ResultsThiopental significantly prolonged atrial ERP in a concentration-dependent manner, whereas propofol and ketamine had no significant effect on atrial refractoriness. In contrast, ketamine caused a dose-dependent decrease in atrial CV, but propofol and thiopental had no significant effect on CV. Therefore, thiopental, ketamine, and propofol caused an increase, a decrease, and no change, respectively, in atrial wavelength. All anesthetics caused a concentration-dependent prolongation of the stimulus-to-His bundle interval, atrioventricular nodal ERP, and WCL. However, on an equimolar basis, significant differences in potencies were found. The concentrations of drug that caused a 20% increase in ERP (ERP20) and WCL (WCL20) for propofol, thiopental, and ketamine were 14+/-2 microM, 26+/-3 microM, and 62+/-11 microM, and 17+/-2 microM, 50+/-1 microM, and 123+/-19 microM (mean+/-SEM), respectively. Therefore, the rank order of potency for frequency-dependent atrioventricular nodal effects is propofol> thiopental> ketamine.ConclusionThe authors' results indicate that propofol would be most effective at filtering atrial impulses during supraventricular tachydysrhythmias, whereas thiopental would be most effective at preventing atrial reentrant dysrhythmias. In contrast, ketamine may be most likely to promote atrial reentry while having minimal effect on atrioventricular nodal conduction.