Rees M, Bowen J C
Ann Surg. 1982 May;195(5):646-52. doi: 10.1097/00000658-198205000-00014.
This study was designed to define the conditions that will consistently produce stress ulcers following the systemic infusion of live E. coli (1.0-1.6 X 10(10) organisms/kg/hr). Using gold-filled oxygen microelectrodes and the in vivo gastric chamber model in dogs, the authors found that the intracellular oxygen tension of the superficial gastric epithelium declined during sepsis despite maintenance of total gastric blood flow. This hypoxia persisted for the three-hour experiment when normal saline bathed the gastric surface (n = 6). Adding 1-mM taurocholate (Tc) (n = 6) or 80-mM hydrochloric acid (HCl) (n = 6) to the gastric chamber improved the cellular hypoxia induced by sepsis, and no ulcers were produced. However, addition of physiologic concentrations of bile in acid (1-mM Tc in 80-mM HCl) produced widespread ulceration of the mucosa within 30 minutes in nine of ten dogs. These experiments demonstrate that epithelial hypoxia induced by sepsis predisposes the gastric mucosa to ulcerate in the presence of physiologic concentrations of topical acid and bile.
本研究旨在确定在全身输注活大肠杆菌（1.0 - 1.6×10¹⁰ 个菌/kg/小时）后持续产生应激性溃疡的条件。作者使用填金氧微电极和犬体内胃腔模型，发现尽管总胃血流量保持不变，但在脓毒症期间浅表胃上皮细胞内的氧张力下降。当用生理盐水冲洗胃表面时（n = 6），这种缺氧在三小时的实验中持续存在。向胃腔中添加1 mM牛磺胆酸盐（Tc）（n = 6）或80 mM盐酸（HCl）（n = 6）可改善脓毒症诱导的细胞缺氧，且未产生溃疡。然而，在酸中添加生理浓度的胆汁（80 mM HCl中含1 mM Tc）在十分之九的犬中于30分钟内导致广泛的黏膜溃疡。这些实验表明，脓毒症诱导的上皮缺氧使胃黏膜在存在生理浓度的局部酸和胆汁时易于发生溃疡。
