Gastric mucosal blood flow and mucosal protection

Prostaglandins (PGs) and omeprazole, both applied intraluminally, have been shown to induce mucosal protion, independently of their inhibitory effects on acid secretion. To investigate the influence of these groups of agents on the gastric mucosal microcirculation, quantitative intravital microscopy of the rat gastric mucosal microcirculation was performed. Single vessel blood flow, calculated from red blood cell velocity and diameter measurements, increased when PGE1, PGE2, 16,16-dimethyl-PGE2, or omeprazole were applied intraluminally. These results suggest that the increase in blood flow may, at least in part, be the reason for the protective action of these substances. A considerably reduced blood flow, such as occurs during hemorrhagic shock, is known to induce gastric bleeding, and also to induce neutrophil adherence to the endothelial wall. Neutrophil antiserum was used to determine whether neutropenia offered protection against hemorrhagic shock-induced gastric bleeding in anesthetized rats. Depletion of neutrophils resulted in higher blood flow during the ischemic period and also attenuated reperfusion-induced gastric damage. Maintenance of blood flow at the same level in untreated rats resulted in a similar reduction of mucosal damage. Thus, the major mechanism by which neutrophils appeared to increase damage in this model of gastric mucosal injury was by increasing microvascular resistance, thereby presumably intensifying tissue hypoxia. This paper is a summary review of previous studies.