Kasten G W, Martin S T
Anesth Analg. 1985 Sep;64(9):911-6.
Using anesthetized dogs, this study compared treatment with lidocaine or bretylium for bupivacaine-induced cardiovascular toxicity. Pentobarbital-anesthetized and -ventilated dogs (n = 10) were given a bolus dose of bupivacaine, 4 mg/kg, and a constant infusion of 0.2 mg X kg-1 X min-1 to produce steady-state serum levels of 7.1 +/- 1.8 microgram/ml of bupivacaine. Using burst ventricular pacing, the ventricular tachycardia threshold was determined, along with hemodynamic and electrophysiologic parameters. The animals were then treated with bretylium, 20 mg/kg (n = 5), or lidocaine, 2 mg/kg, followed by a continuous infusion of lidocaine, 0.1 mg X kg-1 X min-1 (n = 5). Bupivacaine-induced alterations in cardiac output, stroke volume, heart rate, and systemic vascular resistance were corrected by bretylium but not lidocaine. Bupivacaine caused a significant lowering of the ventricular tachycardia threshold, which was consistently raised by bretylium, while lidocaine was either ineffective or caused a further lowering of the threshold. Bupivacaine caused a significant increase in the Q-TU interval and resulted in an undulating polymorphic ventricular tachycardia, similar to that seen in Torsades de Pointes.
本研究使用麻醉犬，比较了利多卡因或溴苄铵对布比卡因所致心血管毒性的治疗效果。戊巴比妥麻醉并通气的犬（n = 10）给予4 mg/kg的布比卡因推注剂量，并以0.2 mg·kg⁻¹·min⁻¹的速度持续输注，以产生布比卡因稳态血清水平7.1±1.8 μg/ml。使用心室猝发起搏，测定室性心动过速阈值以及血流动力学和电生理参数。然后动物接受20 mg/kg的溴苄铵（n = 5）或2 mg/kg的利多卡因治疗，随后以0.1 mg·kg⁻¹·min⁻¹的速度持续输注利多卡因（n = 5）。布比卡因引起的心输出量、每搏输出量、心率和全身血管阻力的改变可被溴苄铵纠正，但不能被利多卡因纠正。布比卡因导致室性心动过速阈值显著降低，而溴苄铵可使其持续升高，利多卡因则无效或导致阈值进一步降低。布比卡因使Q-TU间期显著延长，并导致一种类似于尖端扭转型室速的多形性室性心动过速。
