Effects of halothane on the force of myocardial contraction and energy demand-supply balance (NADH fluorescence) were studied in two rabbit heart preparations--the interventricular septum perfused through the septal artery at various flow levels, and a Langendorff whole-heart preparation with ischemia caused by graded reduction of perfusion pressure. The septum experiments showed that halothane [1.2% = 1.5 minimum alveolar concentration of anesthetic preventing movement response to a noxious stimulus (MAC)] increased NADH fluorescence (+9%, p less than 0.02) at a normal level of perfusion (3 ml/g/min) and, at the same time, decreased it (-6%, p less than 0.02) when myocardial energy balance deteriorated from severe hypoperfusion (0.2 ml/g/min). The inhibitory effect of halothane on developed systolic tension was less pronounced at the low (ischemic) level of myocardial perfusion as compared with the high level--leads to 24% (0.2 ml/g/min) vs. leads to 38% (3 ml/g/min), p less than 0.025. However, if control and halothane values of developed tension were compared at equi-NADH levels (the same state of energy balance), the depressive effect of halothane on the force of myocardial contraction was not less pronounced in severe energy imbalance. Similar results were obtained in the Langendorff preparation experiments. The results suggest that halothane partially restores energy balance in hypoperfused myocardium; however, at the normal level of perfusion, its effect is in an opposite direction. Halothane depresses contractility in the hypoperfused myocardium to a lesser degree than at the normal level of myocardial perfusion. This effect is probably determined by the interaction of two influences: direct depressive effect of the agent on contractile mechanisms, and indirect positive inotropic effect due to improvement in energy balance.