THE ROLE OF ENDOGENOUS ACID IN THE DEVELOPMENT OF ACUTE GASTRIC-ULCERINDUCED BY ISCHEMIA-REPERFUSION IN THE RAT

We investigated the role of endogenous gastric acid in the development of gastric ulcer from erosion induced by ischemia-reperfusion of the celiac artery in the rat. A half-hour clamping of the celiac artery (i schemia) caused acute gastric erosions 1 hour after reperfusion and su ch acute injuries progressed to ulcers 48-72 hours after reperfusion w ithout any necrotizing agents. Gastric acid secretion decreased immedi ately after ischemia and didn't recover until 12 hours after reperfusi on. Intraperitoneal administrations of cimetidine (100 mg/kg, every 12 hours) or omeprazole (30 mg/kg, every 24 hours) were started at 1, 6, or 12 hours after reperfusion. When administrations were started 1 ho ur after reperfusion, both drugs significantly decreased the total dam aged area and prevented the progression of gastric erosions to ulcers. However, administrations started 6 or 12 hours after reperfusion fail ed to inhibit the total damaged area and to prevent ulcer formation. T hese results suggest that endogenous gastric acid may play an importan t role in the progression of gastric erosions to ulcers although ische mia itself reduces acid secretion. Furthermore, treatment with anti-ac id-secretory drugs in the early stage of mucosal damage may be importa nt for the prevention of ulcer. (C) 1997 Elsevier Science Inc.