Gastric blood flow and mucosal defense mechanisms

Recent experimental studies have demonstrated that gastric mucosal blood flow is an essential factor in mucosal defense against acute ulceration. Clinically, most patients who develop stress ulcers have experienced an episode of shock from hemorrhage, sepsis, or cardiac dysfunction. Diminished mucosal blood flow is also a common denominator in animal experiments that employ restraint, hemorrhage, or endotoxemia for the production of acute lesions. The mechanisms by which ischemia produces ulceration have been examined extensively. The leading hypothesis is that gastric mucosal blood flow plays an important role in the disposal, or buffering, of the H+ entering the tissue. Ischemia reduces the capacity of the gastric mucosa to neutralize acid that enters the tissue. This, in turn, leads to accumulation of H+ within the tissue, mucosal acidification, and ulceration. Ischemia may also render the stomach more susceptible to acute ulceration by a severe energy deficit of the gastric mucosa. Using a rat hemorrhagic shock model, a series of experiments demonstrated a profound reduction in mucosal ATP and other high-energy phosphate intermediates that coincided with the development of epithelial cell necrosis. In recent years, many of these experimental observations have been applied clinically in the management of critically ill patients at high risk for development of stress lesions. These include the correction of abnormalities in cardiac output and intravascular volume, careful attention to systemic acid-base balance, adequate nutritional support, and the use of antacids or antisecretory agents. As a result of these preventive measurements, the incidence and prevalence of stress ulcers have decreased significantly in recent years.