We evaluated the hemodynamic effects of amiodarone on left ventricular (LV) function after global ischemia. Amiodarone was administered orally at 15 mg/kg/day for an average of 28 days to a group of 10 dogs. The concentration of amiodarone in serum and LV myocardium was 0.40 ± 0.24 μg/ml and 44 ± 27.0 μg/g, respectively. This experimental group and a control group of 10 dogs each underwent 120 min of aortic cross-clamping with cold crystalloid cardioplegia resulting in an average myocardial temperature of 15°C. LV function measurements by pulse-transit sonomicrometry and Millar solid-state micromanometers were processed by a minicomputer. Compared to the non-treated control group, oral amiodarone for 28 days produced depression of LV contractility which was reflected by lower slope of the end-systolic pressure-volume relation ( Ev max), percentage shortening of segment length, left ventricular pressure-segment length loop area, and slope of the end-systolic pressure-segment length relation ( Es max). After ischemia, percentage recovery of LV global function ( Ev max and mean velocity of circumferential fiber shortening) and regional function ( Es max) was significantly better in the amiodarone group than in the control group. We conclude that oral amiodarone for 28 days results in a depression of LV contractility but the combination of amiodarone and ischemia does not act synergistically to further depress postischemic LV function.