Effects of nitrous oxide on contractile function and metabolism of the isolated heart.

Nitrous oxide has a long clinical history, but its effects on the heart remain controversial. The direct effects of N2O on global myocardial function have not been reported. The authors' aim was to examine the inotropic, chronotropic, dromotropic, and vascular effects of N2O, compared with its N2 control, on hearts isolated from the guinea pig. Hearts (N = 31) were isolated and perfused at 37 degrees C with Krebs-Ringer solution at constant pressure. Isovolumetric left ventricular pressure (LVP) and its derivative (maximum rate of tension development [dP/dtmax]) were measured by placing a saline-filled, latex balloon into the left ventricle. Bipolar electrodes were placed in the right atrium and right ventricle for measurement of heart rate (HR) and atrioventricular conduction time (AVCT). The venae cavae were ligated, and the right ventricle was cannulated through the pulmonic valve to collect coronary sinus effluent for measurement of coronary outflow O2 tension, adenosine, and inosine. After stabilization and perfusion with 96% O2 (plus 4% CO2), each heart was exposed for 10 min either to 48% N2O or to 48% N2 with 48% O2. After repeated perfusion with 96% O2 for 10 min, hearts were exposed in the reverse order to 48% N2O or 48% N2. In the postcontrol period, hearts were again exposed to 96% O2. Inflow Po2 (in mmHg) was 506 +/- 5 (standard error of the mean [SEM]) during 96% O2 and 258 +/- 5 during both 48% N2 and 48% N2O. Effluent Po2 was 155 +/- 7 during 96% O2, 81 +/- 5 during 48% N2, and 83 +/- 5 during 48% N2O.(ABSTRACT TRUNCATED AT 250 WORDS)