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

应激性溃疡发展的病理生理学特别涉及胃粘膜防御机制。

基本信息

批准号：
61571129
负责人：
KITAJIMA Masaki
金额：
$ 1.22万
依托单位：
School of medicine, Kyorin University.
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1986
资助国家：
日本
起止时间：
1986 至 1988
项目状态：
已结题

项目摘要

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.

急性胃粘膜病变（AGML）是众所周知的多种应激的严重并发症。关于应激性溃疡的发展，人们提出了胃酸分泌过多和H^+反向扩散等概念。近年来，对AGML发展的研究重点已从胃粘膜的侵袭性因素转向了防御性因素。本研究旨在探讨应激性溃疡（AGML）发生的机制及合理的治疗方法，并特别关注胃粘膜防御因子。诱导应激（30% B.S.A）后，胃粘膜血流量和ATP合成与假烧伤对照组相比显著减少。血小板聚集也受损。这些结果被认为是胃粘膜防御机制的破坏和AGML发生出血。即腔内H +离子向胃粘膜的反向扩散增加，AGML最终发展为ul。由于H_2受体拮抗剂市售，外科大出血病例的发生率明显降低。但部分对H_2受体拮抗剂治疗无效。通过比较研究来评价手术治疗（迷走神经截尾加幽门成形术）和保守治疗（H_2受体拮抗剂）的合理处理方法。最后，保守治疗并不比手术更有效地改善伴有出血的AGML。结论胃粘膜血流障碍是应激性溃疡发生的重要因素，应选择近全胃切除术而不是迷走神经切开术和幽门成形术。