Gradual reintroduction of oxygen reduces reperfusion injury in cat stomach.

Recent studies have shown that oxygen-derived free radicals are responsible for a major portion of ischemia-reperfusion injury in the stomach. The oxygen radicals are produced during reperfusion when oxygen delivery to the tissue increases. In the present study we investigate the effect on mucosal injury of regulating the rate of reintroduction of oxygen to the stomach after ischemia. Local gastric ischemia was achieved by reducing celiac artery pressure to 30 mm Hg for 1 h. Ischemic injury was assessed by measuring the loss of 51Cr-labeled red blood cells across the gastric mucosa. Mucosal blood loss was negligible before and during the ischemia period but increased to 0.178 ml.min.-1.100 g-1 during reperfusion. When blood flow to the stomach was gradually returned to normal after ischemia by increasing celiac artery pressure by 10 mmHg every 10 min, the mucosal blood loss was reduced to 0.013 ml.min.-1.100 g-1. If the stomach was vascularly perfused with low PO2 (34 mmHg) blood for 1 h after ischemia before being returned to normal arterial perfusion, the mucosal blood loss was also reduced to 0.063 ml.min.-1.100 g-1. When the stomach was made hypoxemic for 1 h rather than ischemic by perfusing the vasculature with low PO2 (29 mmHg) blood then reperfused with normoxic blood, there was very little mucosal bleeding (0.014 ml.min.-1.100 g-1). The data indicate that gastric mucosal bleeding after ischemia is reduced if the tissue is returned slowly to a normal PO2. These findings support the concept that reperfusion injury is due largely to the production of oxygen radicals.(ABSTRACT TRUNCATED AT 250 WORDS)