Acute gastric mucosal lesions induced by vasomotor derangement

Participation of xanthine oxidase and neutrophil-mediated oxidative stress

Abstract

Gastric microcirculatory derangement following intermittent electrical stimuli on the main gastric artery produced many gastric ulcers in rat stomach. In this experimental model, the oxyradical generation from two different sources, xanthine-xanthine oxidase system and local neutrophils, were evaluated.
Laser doppler flowmetry revealed that sharp fluctuation in mucosal blood flow took place during the repeated stimulation, while systemic blood pressure was unchanged. Thirty minutes after the irritation, the decrease in mucosal ATP contents and the increase of hypoxanthine contents were found. Xanthine oxidase activity in the gastric mucosa also elevated simultaneously. Moreover, both ChL activity of an individual neutrophil and mucosal myeloperoxidase activity were dramatically increased. Superoxide dismutase, chlorpromazine and allopurinol significantly inhibited the formation of gastric ulcers, and attenuated both oxyradical generation of neutrophils and xanthine-xanthine oxidase system. The present result suggests that microvascular derangement can cause the increase in oxidative stress mediated by neutrophils and xanthine oxidase system, which may participate in the formation of acute gastric lesions.