Significance of gastric mucosal pepsinogen and plasma corticosteroid levels in the course of cinchophen ulceration.

Abstract

The results reported here have compelling implications concerning gastric mucosal damage in detecting the mechanism of cinchophen-induced gastric lesions in dogs. The acute type of cinchophen gastric lesion, a condition characterized by bleeding and/or diffuse superficial gastric erosions of the fundic gland area, is indicative of so called “stress ulceration” and may be due to activating intramucosal pepsinogen during a rapid increase in endogenous corticosteroid levels. Exogenously administered large doses of corticosteroid or cinchophen solely explained the existence of the correlation between gastric mucosajuice pepsin ratio (MJPR) and the gastric lesion. The greater the increase in MJPR, the greater the change in fundic glandular mucosal destruction. Thus the diffuse superficial mucosal destruction of the fundic gland area, occurring shortly after the medications, was estimated as intramucosal digestion. On the other hand, the chronic cinchophen ulcer in the antral mucosa would be due to both an increased output of gastric pepsin secretion and a decreased mucous secretion which is caused by continuous relatively high basal levels of the steroids. The importance of the role of corticoids in relation to gastric pepsin secretion was sufficiently estimated from the results of MJPR measurements. These findings provide information on the pathogenesis of two types of cinchophen induced gastric lesions.