Nitrous oxide does not depress left ventricular contractility in ischemic rat heart.

The direct effects of nitrous oxide on left ventricular contractility and myocardial oxygen consumption (MVO2) in the ischemic isolated rat heart were studied. The rat heart was isolated and perfused by a Langendorf technique. The aortic stump was cannulated and the heart was perfused with Kumpeis solution bubbled with 95% O2 and 5% CO2 (control phase). A latex balloon was inserted into the left ventricle (LV) to measure LV pressures and dP/dt. Coronary flow was measured and MVO2 was calculated. After the control phase, perfusion pressure was decreased to induce global ischemia (ischemic phase). There were four groups of eight hearts each: control, nitrogen, nitrous oxide, and halothane groups. After 15 min of ischemic phase, the perfusion pressure was increased and the gas mixture was changed to the standard gas mixture (reperfusion phase). Nitrous oxide did not further depress myocardial contractility compared with nitrogen in the ischemic phase, and did not alter MVO2 in the ischemic phase compared with nitrogen. Halothane significantly depressed myocardial contractility and decreased MVO2 in the ischemic phase compared with the control.