Pathophysiology in the development of stress ulcer with special reference to gastric mucosal defensive mechanism.

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Acute gastric mucosal lesions ( AGML ) are wellknown the serious complication of a variety of stresses. Several concepts of the development of stress ulcar have been postulated including gastric acid hypersecretion and H^+ back diffusion. Recently, the focus of investigations on the development of AGML has directed toward from aggressive factor to defensive factor of the gastric mucosa.The purpose of this study was to elucidate the mechanism in the development of AGML ( stress ulcer ) and reasonable therapeutic procedure with special reference to gastric mucosal defensive factor. After induction of stress ( 30 % of B.S.A ), gastric mucosal blood flow and ATP synthesis decreased significantly compared to sham burn control. Platelet aggrigation was also impaired. These results were supposed to be disruption of gastric mucosal defensive mechanism and to occur bleeding from AGML.Namely, intraluminal H^+ ion back diffusion increased to the gastric mucosa and AGML developed ul;timately. since H_2 receptor antagonist was comercially avairable, incidence of surgical cases with massive bleeding significantly decreased. However, some of them was not effective for management with H_2 receptor antagonist. Comparative studies wereperformed to evaluate the resonable managements between surgical ( truncal vagotomy with pyloroplasty ) and conservative ( H_2 receptor antagonist ) treatments.Finally, conservative treatment was not more effective to improve AGML withbleeding than surgery. We concluded that impairment of gastric mucosal blood flow was most important factor in the development of stress ulcer and near total gastrectomy should be selected for surgical treatment of stress ulcer instead of vagotomy and pyloroplasty.