Pathogenesis of NSAID-induced gastric damage: Importance of cyclooxygenase inhibition and gastric hypermotility

Figure 4 Macro- and microscopical observations of gastric lesions induced by indomethacin in rats (A and B) and simultaneous recordings of gastric motility and mucosal blood flow in the rat before and after administration of indomethacin (C). A, B: The animals were given indomethacin (25 mg/kg, s.c.), and the stomachs were excised 4 h later. Note that the lesions were located, in most cases, on the upper part of the mucosal folds (arrow) and in some cases at the base of the folds (arrows); C: Indomethacin (25 mg/kg, s.c.) was given, while atropine (1 mg/kg, s.c.) was given 1 h after indomethacin treatment. Note that during hypermotility states the mucosal blood flow repeated a decrease and an increase, respectively, corresponding to contraction and relaxation of the stomach wall (data from refs. 8 and 33 after modification). GMBF: Gastric mucosal blood flow.