Gastric mucosal blood flow and Escherichia coli bacteremia.

The specific changes in gastric blood flow during sepsis are controversial. Previous investigations of intragastric blood flow using endotoxin models revealed decreased total gastric blood flow and decreased gastric mucosal blood flow. Endotoxin models are now thought to be inadequate due to the accompanying depression of the systemic circulation. More recently, increased gastric blood flow has been demonstrated in a septic hindlimb model. To further elucidate the changes in intragastric blood flow in sepsis, the gastric mucosal and nonmucosal blood flow were measured in the antrum and corpus of pig stomachs before and after the onset of sepsis. Increased gastric mucosal blood flow was demonstrated in both the antrum and corpus 15 minutes after the onset of E. coli bacteremia. By 75 minutes postonset, the changes were not significant, which implied partial recovery. Clinically, gastric mucosal ulcers may accompany the multiple organ system failure of sepsis. These data suggest that mucosal ischemia is not an etiologic factor as previously postulated from experiments with endotoxin.