de La Coussaye J E, Eledjam J J, Peray P, Bruelle P, Lefrant J Y, Bassoul B, Desch G, Gagnol J P, Sassine A
Department of Anaesthesia and Intensive Care, University Hospital of Nîmes, France.
Br J Anaesth. 1993 Oct;71(4):534-9. doi: 10.1093/bja/71.4.534.
We have examined the ability of lemakalim to correct bupivacaine-induced cardiac electrophysiological impairment in an experimental electrophysiological model in closed-chest dogs. Two groups (n = 6) of pentobarbitone-anaesthetized dogs were given atropine 0.2 mg kg-1 i.v., and bupivacine 4 mg kg-1 i.v. over 10 s. Group 2 received also lemakalim 0.03 mg kg-1 i.v. Bupivacaine induced bradycardia, prolonged PR and His-ventricle (HV) intervals, QRS duration, QTc and JTc intervals, decreased left ventricular (LV) dP/dt max and increased LV end-diastolic pressure. Lemakalim reversed bupivacaine-induced PR, HV, QRS, QTc and JTc prolongation, and did not worsen bupivacaine-induced bradycardia and haemodynamic depression. We conclude that lemakalim can antagonize the main deleterious electrophysiological effects induced by a large dose of bupivacaine in anaesthetized dogs.
我们在闭胸犬实验电生理模型中研究了雷马卡林纠正布比卡因诱导的心脏电生理损伤的能力。将两组(每组n = 6)戊巴比妥麻醉的犬静脉注射0.2 mg/kg阿托品,然后在10秒内静脉注射4 mg/kg布比卡因。第2组还静脉注射了0.03 mg/kg雷马卡林。布比卡因诱导了心动过缓,延长了PR间期和希氏束-心室(HV)间期、QRS时限、QTc和JTc间期,降低了左心室(LV)dP/dt max并增加了左心室舒张末期压力。雷马卡林逆转了布比卡因诱导的PR、HV、QRS、QTc和JTc延长,且未加重布比卡因诱导的心动过缓和血流动力学抑制。我们得出结论,雷马卡林可拮抗大剂量布比卡因在麻醉犬中诱导的主要有害电生理效应。