Increased resistance of the rat gastric mucosa to hemorrhagic damage after exposure to an irritant. Role of the "mucoid cap" and prostaglandin synthesis.

This study examined the contribution of the "mucoid cap" that forms on the gastric mucosal surface after the application of an irritant to the increased resistance of the mucosa to damage induced by a subsequent application of ethanol ("adaptive cytoprotection"). Furthermore, the role of prostaglandins in the mechanism of this adaptation was examined. Hemorrhagic necrosis involving greater than 30% of the mucosa was induced by the topical application of 70% ethanol. Exposure of the mucosa to 1 M NaCl before ethanol application resulted in a 98% reduction in hemorrhagic necrosis. Removal of the mucoid cap that formed after application of the NaCl did not cause a reduction of the protective effects. Similarly, pretreatment with indomethacin did not reverse the protection, despite causing a 77% inhibition of gastric cyclooxygenase activity. The present study confirms that the application of an irritant to the gastric mucosa results in a significant increase in the resistance of the mucosa to hemorrhagic damage induced by ethanol. Although the mucoid cap that forms after irritation of the mucosa may play a role in promoting restitution, it does not appear to be responsible for the resistance to hemorrhagic necrosis. Prostaglandin synthesis by the gastric mucosa also does not appear to play a major role in the mechanism of adaptive cytoprotection.