Recombinant human-type SOD attenuates circulatory disorders after reperfusion of splanchnic organs in rats.

Oxygen free radicals (OFRs) have been reported to play pivotal roles in the pathogenesis of cell damage induced by ischemia and reperfusion. The efficacy of recombinant human superoxide dismutase (rh-SOD) in the treatment of circulatory disorders after reperfusion of the splanchnic area was investigated in rats. All rats died within 3 hours after release of 60-min superior mesenteric artery occlusion (SMAO) when no treatment was given. Animals which received rh-SOD, 2 mg.100 g(-1)BW, at reperfusion followed by a continuous infusion of rh-SOD 0.67 mg.100 g(-1)BW.hr(-1), exhibited prolonged survival times compared with no treatment rats (231 +/- 35 min and 149 +/- 43 min, respectively). Mean blood pressure in rats treated with rh-SOD was higher than in controls after reperfusion, and was concomitant with improvement in splanchnic perfusion. The results suggest excessive activity of OFRs in reperfused organs and a possible scavenging effect of rh-SOD as a means of eliminating them.