Halothane-induced decrease in experimental myocardial ischemia in the non-failing canine heart.

The effect of halothane on net myocardial oxygen balance of ischemic myocardium was studied in the non-failing canine heart. Myocardial ischemia was produced by repeated reversible occlusions of a coronary artery; the severity of ischemia was estimated by summating ST-segment elevations (sigma ST) obtained by epicardial ECG mapping at 15 to 18 sites. Control measurements were obtained before and after administration of halothane (0.75 per cent) to six dogs with chloralose-urethane basal anesthesia. Halothane was associated with significant decreases of systemic arterial pressure (P less than .001), heart rate (P less than .01), and the product of systolic arterial pressure X heart rate (P less than .01), an indirect index of myocardial oxygen consumption, while left atrial pressure remained unchanged at normal levels. sigmaST during occlusion was less (P less .001) during halothane (26.5 +/- 7.4 (SD) mv) than before (36.6 +/- 5.4 mv) or after (34.4 +/- 8.2 mv) its administration. Thus, halothane decreased the severity of experimentally-induced myocardial ischemia in the non-failing canine heart. The data suggest that, in the absence of ventricular failure, halothane influences the relationship between myocardial oxygen supply and demand in a favorable direction when coronary blood flow is limited.