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几种酰胺类局部麻醉药对麻醉犬的电生理和血流动力学影响的比较

Comparative electrophysiologic and hemodynamic effects of several amide local anesthetic drugs in anesthetized dogs.

作者信息

Bruelle P, LeFrant J Y, de La Coussaye J E, Peray P A, Desch G, Sassine A, Eledjam J J

机构信息

Department of Anesthesiology, Critical Care, and Emergency, University-Hospital of Nîmes, Montpellier, France.

出版信息

Anesth Analg. 1996 Mar;82(3):648-56. doi: 10.1097/00000539-199603000-00038.

Abstract

Large and equipotent doses of several local anesthetics were administered in a cardiac electrophysiologic model on closed-chest dogs. Five groups of pentobarbital-anesthetized dogs were each given intravenously 16 mg/kg lidocaine, 12 mg/kg mepivacaine, 4 mg/kg or 8 mg/kg etidocaine, and 4 mg/kg bupivacaine. Lidocaine induced bradycardia, slowing of atrioventricular node conduction (AH), and marked hemodynamic depression, represented by a decrease in mean aortic pressure (MAoP), in the peak of first derivative of left ventricular pressure (LVdP/dt(max)) and by an increase in left ventricular end-diastolic pressure (LVEDP). Atrial pacing at pacing cycle length (PCL) of 298 ms did not enhance the alteration of variables of ventricular conduction (His ventricle [HV] interval and QRS duration). Mepivacaine induced slight alteration of electrophysiologic variables. Atrial pacing at PCL of 312 ms did not enhance the alteration of HV and QRS duration. Mepivacaine induced transient hemodynamic depression. Etidocaine (4 mg/kg) induced electrophysiologic and hemodynamic alterations similar to mepivacaine but artrial pacing at PCL of 330 ms enhanced HV lengthening and QRS widening (P < 0.05). Etidocaine (8 mg/kg) induced marked impairment of PR, HV, QRS, and QT, and dramatic hemodynamic depression represented by a decrease in MAoP from 123.5 +/- 16.2 at baseline to 36.5 +/- 8.3 mm Hg at 1 min (P < 0.001) and of LVdP/dtmax) from 1446 +/- 379 to 333 +/- 93 mm Hg/s (P < 0.001). Bupivacaine induced dramatic impairment of electrophysiologic variables. Bupivacaine also decreased LVDP/dtmax (from 1333 +/- 347 to 617 +/- 299,P < 0.001) and increased LVEDP. We conclude that mepivacaine induced moderate cardiotoxicity. In contrast, lidocaine induced dramatic hemodynamic depression while etidocaine and bupivacaine markedly impaired both electrophysiologic and hemodynamic variables. This double impairment could explain the great difficulty in resuscitating patients who have had cardiotoxic accidents induced by etidocaine or bupivacaine.

摘要

在封闭胸腔犬的心电生理模型中给予几种大剂量且等效的局部麻醉药。五组戊巴比妥麻醉的犬分别静脉注射16mg/kg利多卡因、12mg/kg甲哌卡因、4mg/kg或8mg/kg依替卡因以及4mg/kg布比卡因。利多卡因引起心动过缓、房室结传导减慢(AH)以及明显的血流动力学抑制,表现为平均主动脉压(MAoP)降低、左心室压力一阶导数峰值(LVdP/dt(max))降低以及左心室舒张末期压力(LVEDP)升高。在起搏周期长度(PCL)为298ms时进行心房起搏,并未增强心室传导变量(希氏束-心室[HV]间期和QRS时限)的改变。甲哌卡因引起电生理变量的轻微改变。在PCL为312ms时进行心房起搏,并未增强HV和QRS时限的改变。甲哌卡因引起短暂的血流动力学抑制。依替卡因(4mg/kg)引起的电生理和血流动力学改变与甲哌卡因相似,但在PCL为330ms时进行心房起搏可增强HV延长和QRS增宽(P<0.05)。依替卡因(8mg/kg)引起PR、HV、QRS和QT的明显损害以及显著的血流动力学抑制,表现为MAoP从基线时的123.5±16.2mmHg在1分钟时降至36.5±8.3mmHg(P<0.001),LVdP/dt(max)从1446±379降至333±93mmHg/s(P<0.001)。布比卡因引起电生理变量的显著损害。布比卡因还降低了LVDP/dtmax(从1333±347降至617±299,P<0.001)并升高了LVEDP。我们得出结论,甲哌卡因引起中度心脏毒性。相比之下,利多卡因引起显著的血流动力学抑制,而依替卡因和布比卡因则显著损害电生理和血流动力学变量。这种双重损害可以解释在抢救因依替卡因或布比卡因导致心脏毒性事故的患者时所面临的巨大困难。

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