The cardiotonic agent amrinone does not increase anatomic infarct size.

The effect of the positive inotropic agent amrinone on anatomic infarct size induced by coronary artery occlusion and reperfusion in dogs is unknown, although previous studies have shown that amrinone increases indices of myocardial ischemia during very brief coronary artery occlusions. Thus, this study was performed to determine if amrinone changes anatomic infarct size and improves hemodynamics induced by 3 h of coronary occlusion and 3 h of reperfusion in anesthetized, open-chest dogs. Amrinone (1-mg/kg bolus followed by 6 mg/kg/h) or an equivalent volume of saline was administered intravenously for 3 h beginning 30 min postocclusion. The area at risk was 19.7 +/- 2.6% in the control group (n = 9) and 20.2 +/- 1.8% in the amrinone-treated group (n = 9; p = NS). The amount of the area at risk that developed infarction was 60.6 +/- 6.1% in the control group and 54.6 +/- 5.6% in the amrinone-treated group (p = NS). Pretreatment left ventricular end-diastolic pressure increased from 11.4 +/- 1.8 to 20.1 +/- 3.0 mm Hg (p less than 0.05) in the control group and from 10.8 +/- 1.3 to 17.3 +/- 1.3 mm Hg (p less than 0.05) in the amrinone-treated group following coronary artery occlusion. During coronary occlusion, amrinone administration significantly increased left ventricular maximum +dP/dt [+483 +/- 85 vs. -11 +/- 53 mm Hg/s (p less than 0.01) in amrinone vs. control group, respectively] and heart rate (+27 +/- 6 vs. -4 +/- 2 beats/min; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)