Comparative pathophysiology of nonglandular ulcer disease: a review of experimental studies.

Abstract

Ulceration of the nonglandular, stratified squamous mucosa of the equine and porcine stomach is a common event in both species, although in pigs the fatality rate is significant and it is an economically important disease. Because the barrier function of this mucosa in horses and pigs appears similar, it is probable that similar pathophysiological mechanisms may be responsible for the initiating lesions and reparative events. Recent studies of ulcer pathogenesis in the pig have shown that feed preparation or prolonged fasting can result in disruption of the normal stratification of gastric contents, thereby allowing high concentrations of HCl, pepsin and refluxed bile to mix in the proximal stomach. Conditions simulating those found in vivo have been shown to damage this mucosa in vitro and indicate that luminal products, such as short chain fatty acids and bile salts, which act in synergy with HCl, probably are necessary to induce significant damage to this mucosa. Studies of the equine stomach have shown a similar proximal to distal pH gradient in the fed stomach, a significant duodenal-gastric reflux, and induction of squamous ulcers with fasting, thereby illustrating that similar conditions may be responsible for damage to the equine nonglandular mucosa.