Experimental ischemia of 15, 30, or 60min length, followed by 30 min of reperfusion, was produced in situ in the cat small intestine by means of an adjustable arterial clamp. Arterial perfusion pressure was lowered to such an extent that intestinal blood flow decreased from about 25 to 3.5 ml × min–1 × 100 g–1. The rate of free radical formation was followed intermittently with ESR and a modified spin trapping technique in the control period prior to ischemia and at various times during reperfusion. Upon reperfusion radical formation increased above the preischemic control value in all three series of experiments. Cumulative radical production during the 30 min reperfusion period rose from about 3 µmol × 100 g–1 after 15 min ischemia to approximately 4.5 µmol × 100 g–1after 30 min and 8-10 µmol × 100 g–1 after 60 or 120 min ischemia. At the same time mucosal damage became more pronounced, suggesting a causal connection between tissue damage and radical formation. More specifically, radical production was strongly correlated to histological damage occurring during reperfusion as seen when comparing radical production in animals not experiencing reperfusion damage to those who did. Radical formation in these two groups were 0.35 and 9.0 µmol × 100 g–1, resp