Gastric injury induced by hemorrhage, local ischemia, and oxygen radical generation.
Gastric mucosal injury caused by local intra-arterial generation of oxygen-derived free radicals was compared with gastric injury caused by 30 min of hemorrhage-induced ischemia (systemic pressure of 30 mmHg) or local ischemia (celiac artery pressure of 30 mmHg). The index of injury was the loss of 51Cr-labeled red cells across the gastric mucosa. Generation of oxygen radicals in the celiac artery caused a rapid increase in mucosal blood loss during the period of radical generation (0.029 +/- 0.013 ml X min-1 X 100 g-1, mean +/- SE), and this loss was maintained after radical production ceased (0.041 +/- 0.018 ml X min-1 X 100 g-1). Local ischemia produced similar mucosal injury; however, this occurred after reperfusion of the stomach (0.038 +/- 0.006 ml X min-1 X 100 g-1) and not during the ischemic episode (0.001 +/- 0.0003 ml X min-1 X 100 g-1). Hemorrhage-induced ischemia produced a threefold greater mucosal blood loss (0.133 +/- 0.048 ml X min-1 X 100 g-1) than local ischemia. The results of this study indicate that oxygen radicals generated enzymatically in the blood supply to the stomach cause mucosal bleeding of similar magnitude to that observed after local ischemia and that gastric ischemia induced by systemic hypotension produces more severe gastric injury than the same level of local hypotension.
D000818:Animals; D005260:Female; D005609:Free Radicals; D006470:Hemorrhage / Q000473:pathology*; D007511:Ischemia / Q000473:pathology*; D008297:Male; D009929:Organ Size; D010100:Oxygen / Q000096:biosynthesis*; D051381:Rats; D013270:Stomach / Q000098:blood supply* / Q000473:pathology
D005609:Free Radicals; D010100:Oxygen