Stress Ulcers during Live Escherichia coli Sepsis

Abstract

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 10¹⁰ 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 (HCI) (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 HCI) 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.