Gallenberg L A, Stowe D F, Kampine J P, Bosnjak Z J
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee.
Anesthesiology. 1993 Jun;78(6):1112-9; discussion 23A-24A. doi: 10.1097/00000542-199306000-00014.
Calcium channel blockers and volatile anesthetics have depressant effects on cardiac function. Both groups of drugs appear to exert both qualitatively and quantitatively different effects on electrophysiologic and mechanical function. The aim of this study was to compare the direct cardiac effects of the calcium channel blocker nifedipine in the absence and presence of isoflurane, halothane, or enflurane.
Guinea pig hearts (N = 36) were isolated and perfused with oxygenated Krebs-Ringer solution (pH 7.4, 37 degrees C). Recording electrodes were placed in the right atrium and ventricle to measure heart rate and atrioventricular (AV) conduction time. Isovolumetric left ventricular pressure (LVP) was measured via a latex balloon and transducer. Hearts were randomly assigned to one of three anesthetic groups at 0.7 and 1.4 minimum alveolar concentration (MAC) and treated with 15 and 30 nM nifedipine.
Nifedipine alone significantly decreased atrial rate and left ventricular pressure, without prolonging AV conduction. Nifedipine plus isoflurane, halothane, or enflurane did not significantly prolong AV conduction compared with the respective anesthetic agent alone, but nifedipine plus isoflurane, halothane, or enflurane significantly decreased atrial rate compared with the effect of the anesthetic alone. Halothane or enflurane plus nifedipine significantly decreased atrial rate more than nifedipine alone or isoflurane plus nifedipine. Isoflurane, halothane, or enflurane plus nifedipine significantly depressed LVP more than the respective anesthetic agent alone. Halothane or enflurane plus nifedipine also significantly depressed LVP more than isoflurane plus nifedipine or nifedipine alone.
This study demonstrates that the combined treatment of nifedipine and volatile anesthetics, especially enflurane, additively depresses atrial rate and contractility, but not AV conduction in vitro. In comparison with results reported previously, these effects appear less pronounced than those of the combination of volatile agents with diltiazem and, especially, verapamil.
钙通道阻滞剂和挥发性麻醉药对心脏功能有抑制作用。这两类药物似乎在电生理和机械功能方面产生了质和量上不同的影响。本研究的目的是比较在不存在和存在异氟烷、氟烷或恩氟烷的情况下钙通道阻滞剂硝苯地平对心脏的直接作用。
分离36只豚鼠心脏,用含氧的 Krebs-Ringer 溶液(pH 7.4,37℃)灌注。记录电极置于右心房和心室以测量心率和房室(AV)传导时间。通过乳胶气球和换能器测量等容左心室压力(LVP)。心脏随机分配到三个麻醉组之一,浓度分别为0.7和1.4最低肺泡浓度(MAC),并用15和30 nM硝苯地平处理。
单独使用硝苯地平可显著降低心房率和左心室压力,而不延长房室传导。与单独使用相应麻醉剂相比,硝苯地平加异氟烷、氟烷或恩氟烷并未显著延长房室传导,但与单独使用麻醉剂的效果相比,硝苯地平加异氟烷、氟烷或恩氟烷显著降低了心房率。氟烷或恩氟烷加硝苯地平比单独使用硝苯地平或异氟烷加硝苯地平更显著地降低心房率。异氟烷、氟烷或恩氟烷加硝苯地平比单独使用相应麻醉剂更显著地降低左心室压力。氟烷或恩氟烷加硝苯地平也比异氟烷加硝苯地平或单独使用硝苯地平更显著地降低左心室压力。
本研究表明,硝苯地平和挥发性麻醉药联合治疗,尤其是恩氟烷,在体外可累加性地降低心房率和收缩力,但不影响房室传导。与先前报道的结果相比,这些作用似乎不如挥发性药物与地尔硫卓尤其是维拉帕米联合时明显。