Oxygen free radicals contribute to postburn cardiac cell membrane dysfunction.

This study evaluated the contribution of O2 free radicals to changes in cardiac function after burn injury. Full-thickness scald burns comprising 42% of the total body surface area were produced in rats. Mean arterial pressure, heart rate, pH, cardiac transmembrane potential (Ling Gerard electrode, Em), myocardial ATP, creatine phosphate (CP), glucose 6-phosphate, and lactate were measured enzymatically 24 hr postburn in four groups: Group 1, sham burn controls, N = 12; Group 2, untreated burn injury, N = 14; Group 3, N = 10, burn injury resuscitated with Ringer's lactate (Parkland formula); Group 4, burns pretreated with oral allopurinol (10 mg/kg) for 5 days before burn injury, N = 11. In vitro cardiac contractile function was assessed 24 hr after burn injury in additional animals (N = 8) from each of the four experimental groups. Untreated burn injury caused hypotension, bradycardia, depolarization of the cardiac cell membrane (Em fell from 78.5 +/- 0.4 to 66.8 +/- 0.4, P < 0.05), and left ventricular contractile depression despite no significant fall in cardiac ATP content. In contrast, cardiac tissue CP fell and myocardial tissue lactate rose. Allopurinol pretreatment oblated burn-induced hypotension, bradycardia, and cardiac cell membrane depolarization and improved cardiac contractile function despite no fluid resuscitation from burn injury. In contrast, aggressive fluid resuscitation from burn injury (Group 3) repolarized cardiac cell membrane but did not reverse burn-induced cardiac contractile deficits. These data suggest that xanthine oxidase-mediated free radical production contributes, in part, to postburn alterations in cardiac function.