In the last decade, significant progress has been made in understanding the basic mechanisms involved in the development of acute stress gastritis. Many of the experimental observations have been applied in our clinical approaches to patients at high risk. A strong impression exists among investigators that efforts to improve ventilatory support, correct abnormalities in cardiac output and intravascular volume, and maintain adequate nutrition in critically ill patients may have contributed to the decreased incidence and prevalence of stress gastritis over the past decade. In addition, reduction of intragastric acidity, either by titration with antacids or administration of H2 antagonists, further prevented stress gastritis in these patients. We have every reason to believe that progress will continue at the same rate in the decades before us in this area of investigation.