Control of hemodynamics prevents worsening of myocardial ischemia when nitrous oxide is administered to isoflurane-anesthetized dogs.

Abstract

This study was designed to determine if nitrous oxide can worsen myocardial ischemia by directly affecting coronary tone in the absence of changes in myocardial oxygen consumption. Three anesthetics were compared in each animal: isoflurane 1.8% alone, isoflurane 1.4% with 50% nitrous oxide, and isoflurane 1.8% with 50% nitrous oxide. Heart rate, systolic aortic pressure and left atrial pressure were held constant during the three treatments. In 12 isoflurane-anesthetized dogs the chest was opened and the left anterior descending (LAD) coronary artery cannulated and perfused with an autoperfusion circuit. Systolic segment shortening was measured in the LAD circumflex regions of the heart with a sonomicrometer. Regional myocardial blood flow was measured with radioactive microspheres. Measurements were made during imposition of a stenosis on the perfusion circuit sufficient to decrease systolic shortening by 30-50%. The same stenosis was imposed three times in a randomized and balanced crossover design. When heart rate, blood pressure, and left atrial pressure were held constant, the substitution of 50% nitrous oxide for 0.4% isoflurane had no effect on myocardial blood flow or function in the ischemic or normal region. When nitrous oxide was added to 1.8% isoflurane, systolic shortening decreased by 35% in the ischemic and 27% in the normally perfused region, but myocardial blood flow was unaffected. The decrease in shortening was therefore not due to increased ischemia. The effects of nitrous oxide on ischemic myocardium can be explained by its well-known hemodynamic and direct myocardial actions. These results suggest that nitrous oxide does not have important direct effects on the coronary circulation.