Effects of hypertonic sodium chloride solution on the electrophysiologic alterations caused by bupivacaine in the dog heart.

The effects of various hypertonic solutions on the intraventricular conduction, ventricular repolarization and the arrhythmias caused by the intravenous (iv) injection of bupivacaine (6.5 mg/kg) were studied in sodium pentobarbital-anesthetized mongrel dogs. Hypertonic solutions, given iv 5 min before bupivacaine, were 7.5% (w/v) NaCl, 5.4% (w/v) LiCl, 50% (w/v) glucose (2,400 mOsm/l, 5 ml/kg), or 20% (w/v) mannitol (1,200 mOsm/l, 10 ml/kg). Bupivacaine induced severe arrhythmias and ventricular conduction and repolarization disturbances, as reflected by significant increases in QRS complex duration, HV interval, IV interval and monophasic action potential duration, as well as severe hemodynamic impairment. Significant prevention against ventricular electrophysiologic and hemodynamic disturbances and ventricular arrhythmias was observed with 7.5% NaCl (percent increase in QRS complex duration: 164.4 +/- 21.8% in the non-pretreated group vs 74.7 +/- 14.1% in the pretreated group, P<0.05; percent increase in HV interval: 131.4 +/- 16.1% in the non-pretreated group vs 58.2 +/- 7.5% in the pretreated group, P<0.05; percent increase in monophasic action potential duration: 22.7 +/- 6.8% in the non-pretreated group vs 9.8 6.3% in the pretreated group, P<0.05; percent decrease in cardiac index: -46 6% in the non-pretreated group vs -28 +/- 5% in the pretreated group, P<0.05). The other three hypertonic solutions were ineffective. These findings suggest an involvement of sodium ions in the mechanism of hypertonic protection.

Effects of hypertonic sodium chloride solution on the electrophysiologic alterations caused by bupivacaine in the dog heart

The effects of various hypertonic solutions on the intraventricular conduction, ventricular repolarization and the arrhythmias caused by the intravenous (iv) injection of bupivacaine (6.5 mg/kg) were studied in sodium pentobarbital-anesthetized mongrel dogs. Hypertonic solutions, given iv 5 min before bupivacaine, were 7.5 percent (w/v) NaCl, 5.4 percent (w/v) LiCl, 50 percent (w/v) glucose (2,400 mOsm/l, 5 ml/kg), or 20 percent (w/v) mannitol (1,200 mOsm/l, 10 ml/kg). Bupivacaine induced severe arrhythmias and ventricular conduction and repolarization disturbances, as reflected by significant increases in QRS complex duration, HV interval, IV interval and monophasic action potential duration, as well as severe hemodynamic impairment. Significant prevention against ventricular electrophysiologic and hemodynamic disturbances and ventricular arrhythmias was observed with 7.5 percent NaCl (percent increase in QRS complex duration: 164.4 ± 21.8 percent in the non-pretreated group vs 74.7 ± 14.1 percent in the pretreated group, P<0.05; percent increase in HV interval: 131.4 ± 16.1 percent in the non-pretreated group vs 58.2 ± 7.5 percent in the pretreated group, P<0.05; percent increase in monophasic action potential duration: 22.7 ± 6.8 percent in the non-pretreated group vs 9.8 ± 6.3 percent in the pretreated group, P<0.05; percent decrease in cardiac index: -46 ± 6 percent in the non-pretreated group vs -28 ± 5 percent in the pretreated group, P<0.05). The other three hypertonic solutions were ineffective. These findings suggest an involvement of sodium ions in the mechanism of hypertonic protection