Abstract
The stress ulcers that occur in shocked dogs are averted by pyloric cross-clamping prior to shock. These experiments studied the role of bile reflux in the pathogenesis of stress ulcers in the shocked dog. Two and one-half hours of hemorrhagic shock in dogs with acute antral pouches isolated from the duodenum did not alter antral mucosal integrity as measured by gastric mucosal volume and ionic flux rates despite a fall in transgastric potential difference (PD) indicating mucosal injury (-33.5 +/- 1.7 m Volts vs -12.8 +/- 2.0, p < 0.01). Similarly 4(1/2) hours of shock did not alter mucosal integrity when the pylorus was cross-clamped during shock (PD -59.8 +/- 1.8 mV vs -42.5 +/- 7.0, p = 0.05). In contrast, 4(1/2) hours of shock in dogs in whom the pylorus was open resulted in increased hydrogen ion back diffusion (-106.3 +/- 21.5 microEq vs -300.5 +/- 63.1, p < 0.01, PD -56.8 +/- 3.6 mV vs -24.3 +/- 3.4, p < 0.01). The concentration of bile acids refluxed into the stomach during unmodified shock (8.45 +/- 3.92 mM) exceeds that necessary to disrupt the gastric mucosal barrier. These data suggest that increased hydrogen ion back diffusion initiated by refluxed bile plays an important role in the pathogenesis of gastric stress ulcers in the shocked dog.