Gastric acid secretion and mucosal defense mechanisms with special reference to the role of cimetidine in critically ill patients

Abstract

The gastromucosal barrier (GMB) can be disrupted by a number of aggressive factors or by a decrease in mucosal defense factors. If there is back diffusion of hydrogen ions into the mucosa, mucosal damage ranging from an erythematous gastro-duodenitis to erosive and ulcerative gastritis or life-threatening hemorrhage may ensue. The pathogenesis of stress-related mucosal damage seen in critically ill patients suffering from burns, sepsis, head trauma, respiratory insufficiency, or multisystem disease is also related to a decrease in mucosal resistance. Early studies of cimetidine in animals and in humans demonstrated its ability to increase gastric transmucosal potential difference, indicating an enhancement of the integrity of the GMB. Several studies show that cimetidine protects the stomach from aspirin-induced mucosal damage; increases gastric mucus production and mucus glycoprotein content, which contributes to the protective action of mucus; increases mucosal secretion of bicarbonate; increases gastric mucosal blood flow, which prevents mucosal hypoxia seen in patients in shock or otherwise critically ill patients; increases endogenous mucosal prostaglandin synthesis; and increases the rate of epithelial cell renewal, a factor important to mucosal healing. Since cimetidine suppresses acid secretion and enhances mucosal defense, it is an important therapeutic tool in the management of acid-related disorders, particularly stress-related mucosal damage.