Comparison of approaches to stress ulcer prophylaxis in hemorrhagic shock

Abstract

Stress ulceration can be prevented clinically by prophylaxis with antacids or sucralfate, while hyperosmolar glucose and prostaglandins have prevented gastric mucosal injury in experimental models. We compared these four agents' effectiveness in gastric mucosal protection as well as their interaction with the pathophysiology of hemorrhagic shock. Gastric mucosal injury was produced in a canine model with the insults important in clinical situations: intragastric acid, intragastric bile, and gastric mucosal ischemia. Hypotension was maintained at a constant level for 3 hr, during which one of the prophylactic treatments or vehicle (H 2O) was given hourly intragastrically. The stomachs were harvested for quantification of gastric mucosal injury after return of shed blood. The percentage of gastric area damaged was significantly decreased to 1.0 ± 0.7% by antacids but was increased to 43.5 ± 4.9% by 16,16-dimethyl prostaglandin E 2 (16,16-dmPGE 2), in comparison to vehicle treatment which caused 28.4 ± 4.7% lesioned mucosa. Additionally, hemodynamic function differed between treatment groups after 1 hr of shock. Irrespective of treatment group, parameters reflecting volume status and hemodynamic function correlated significantly with the amount of gastric mucosal injury measured in individual animals. Intragastric treatments did not variably affect systemic pH or systemic glucose, and neither of these parameters was related to gastric mucosal injury. In conclusion, antacids effectively prevent stress ulceration in canine hemorrhagic shock, while the worsening of gastric mucosal injury and hemodynamic function we observed with 16,16-dmPGE 2 treatment indicates that this agent could be hazardous in hypotensive patients.