Free radical formation during splanchnic artery occlusion shock.

Abstract

Free radical (FR) formation in the rat intestinal lumen was measured using the spin-trapping technique and electron paramagnetic resonance spectroscopy. Intestinal ischemia was produced by occluding the celiac and the superior mesenteric arteries for 30 min followed by reperfusion. The lumen was filled with a solution of PBN (N-tert-butyl-alpha-phenyl-nitrone) and the intestine was squeezed to enhance the interaction between the PBN solution and the intestinal mucosal cells. Free radicals were produced upon reperfusion, with peaks at 5 and 90 min. Post-ischemic treatment with superoxide dismutase (20 mg.kg(-1)) inhibited the increase of FR production during the second peak by 36%. In a single study in a group of leucocytopenic rats (WBC < 1500/mm(3)), the increase of FR production during the second peak was decreased by 80%. However, these treatments did not inhibit the FR production during the first peak in either group. In contrast, pretreatment with allopurinol (40 and 100 mg.kg(-1) injection at 24 and 3 hours before ischemia, respectively) inhibited the FR production during the first peak by 76%, but did not inhibit during the second peak. The changes in lipid peroxidation in the intestinal mucosa, specific gravity of the intestine and in the hematocrit were correlated to the FR production in the second peak. These results suggest that a major cause of tissue injury after reperfusion in the ischemic intestine may largely be produced by neutrophils.