Gastric Pathology (16-Dec-2003)

Gastric Ulceration in the Adult Gastric ulceration syndrome (GUS), a complicated and multi-factorial problem, is a common disorder of the stomach of mature horses. Horses that are turned out to pasture and are not involved in work have normal stomachs as do most horses used for light work or pleasure (Murray 1994). In recent years the widespread nature of this disorder has gained increased recognition and studies have shown that racing horses and horses in race training have a high prevalence of gastric ulcers with estimates ranging from 66 per cent (Hammond et al. 1986) to over 90 per cent (Murray 1994). Horses used for pleasure have a lower prevalence (37 per cent) and severity of ulcers (Murray et al. 1989). It has been suggested that the prevalence and severity of gastric ulcers increase with the duration of race training. Prevalence in a randomly selected group of normal thoroughbred horses in race training was 28 per cent at the start of the study and 63 per cent with ongoing racing and training (Orsini and Pipers 1997). GUS is due to an imbalance between mucosal aggressive factors (hydrochloric acid, pepsin, bile acids and organic acids) and mucosal protective factors (bicarbonate and mucus). The equine stomach is lined dorsally by a stratified squamous epithelium and ventrally by a glandular epithelium. These epithelia have different functions and different susceptibilities to peptic injury. The squamous portion of the stomach appears to serve as a reservoir for ingesta and has no secretory or absorptive function. Because its mucosa has no surface barrier to hydrochloric acid, its protection from peptic injury depends on limited exposure to acidic gastric secretions. In contrast the glandular mucosa has more protective factors and may have different causes for ulceration. It secretes hydrochloric acid and pepsin as well as some water and electrolytes, and a variety of endocrine mediators are produced within this mucosa. The gastric glandular mucosa has evolved elaborate mechanisms to protect itself from peptic injury including a mucus/bicarbonate barrier that prevents back diffusion of hydrochloric acid, mucosal blood flow, cellular restitution and growth factors that promote mucosal healing. Prostaglandin E2 promotes secretion of the mucus/bicarbonate layer and enhances mucosal blood flow, mucus and bicarbonate production. Consequently, inhibiting prostaglandin synthesis decreases mucosal blood flow and mucus and bicarbonate secretion and increases gastric acid secretion by the glandular mucosa. Prostaglandins may provide additional protection by helping to maintain the integrity of the glandular and non-glandular mucosa by stimulation of surface-protective phospholipids, enhancement of mucosal repair and prevention of cell swelling by stimulation of sodium transport. The stress of training and confinement in adult horses may lead to the exogenous release of corticosteroids which can inhibit prostaglandin synthesis. This decrease in prostaglandin synthesis may lead to breakdown of mucosal protective factors. The equine stomach secretes hydrochloric acid continuously even when the horse is not eating. Gastric acidity is least when the horse is eating because eating stimulates secretion of bicarbonate-rich saliva that can neutralise some gastric acid, and roughage absorbs gastric secretions so that they do not contact the mucosal surface. Once a horse stops eating, gastric acidity can rapidly increase, with pH falling below 2.0 and acidity remaining high while the horse does not eat.