Restraint-induced gastric erosions. Role of acid back diffusion.

Abstract

Disruption of the gastric mucosal barrier to back diffusion of hydrogen ions has been postulated as an etiologic factor in stress-induced acute gastric mucosal lesions. This hypothesis was tested in rats subjected to restraint stress for 0, 1, 4, and 24 hours. One hour prior to the cessation of restraint and sacrifice, the pylorus was ligated and a test solution instilled into the stomach. The test solution contained either H+ 100 mEq/liter or isotonic saline. In calculating the net flux of hydrogen ion in the acid test groups, hydrogen ion secretion was corrected for in one of two ways: 1) the volume distribution of sodium in the gastric contents (based on Hollander's two-component hypothesis) or 2) the mean secretion of hydrogen ion in similarly treated saline-instilled rats. With either method, all rats showed back diffusion, and there was no difference in the extent of back diffusion between control and stressed animals. Not even in the presence of multiple acute gastric mucosal lesions, in rats subjected to prolonged restraint, was there an increase in back diffusion as compared with control values. The presence of mucosal lesions was correlated with the presence of hydrogen ions and the length of restraint stress but not with any change in hydrogen ion back diffusion. In the restrained pylorus-ligated rats, there was a marked decrease in hydrogen ion secretion; this may represent a protective mechanism. No evidence was found to support the original hypothesis.