Depression of pancreatic bicarbonate response during endotoxic shock in dogs

Abstract

Upper gastrointestinal erosions have been a significant clinical finding subsequent to septic or endotoxic shock. Gastric acid as an integral factor in the stress ulcer syndrome is crucial to the formation of acute gastric erosions both in man [8] and in the dog [4]. Recent experiments have demonstrated that endotoxin-induced shock severely reduces the ability of the canine proximal duodenum to clear or neutralize hydrochloric acid (HCl) [21. The two main mechanisms by which HCl is cleared from the duodenum are neutralization by pancreatic bicarbonate (HCO,), and transmural absorption of the hydrogen ion [9]. Greenberg and Himal [2] noted a significant decrease in both the amount of hydrogen ion lost transmurally and in the amount neutralized and diluted by mixed bile and pancreatic juice secretions in canine duodenal pouches during endotoxic shock. This decreased clearance was associated with the formation of acute duodenal erosions. The following experiments were done with the intent of quantitating the role of the pancreas in the neutralization of HCl during endotoxic shock in dogs.