Efficacy of recombinant-derived human superoxide dismutase on porcine left ventricular contractility after normothermic global myocardial ischemia and hypothermic cardioplegic arrest. A porcine model of normothermic global ischemia (40 minutes) followed by systemic cooling to 25 degrees C with 4 degrees C crystalloid cardioplegic arrest (90 minutes) was used to assess the efficacy of recombinant-derived human superoxide dismutase (r-HSOD) on postreperfusion left ventricular function while on cardiopulmonary bypass. Isovolumic hemodynamic function was monitored, and adenine nucleotide pool was measured in myocardial biopsy specimens and coronary sinus effluent. The treatment group of pigs (n = 7) received 15 mg/kg r-HSOD immediately before warm reperfusion, both left ventricular peak systolic pressure and developed pressure were significantly better in the r-HSOD group of pigs (p less than 0.05 vs. placebo). This improvement persisted at 60 minutes of reperfusion (p less than 0.05 vs. placebo). Myocardial ATP and total adenine nucleotides did not differ, nor did adenine nucleotide catabolites in the coronary sinus effluent differ between treatment groups of pigs. The exception to this was the nucleotide catabolite inosine, which was significantly elevated in coronary sinus effluent of pigs treated with r-HSOD at 30 minutes of reperfusion (p less than 0.05 vs. placebo). In this model of global ischemia and reperfusion, a recombinant-derived human free-radical scavenger provides significant protection of systolic but not diastolic function. Values for myocardial ATP and total adenine nucleotide content suggest that the improvement in mechanical function during reperfusion is not due to enhanced preservation of myocardial bioenergetics. 