Pressure injury to the gastric mucosa: Studies on an in vivo model of acute gastric dilatation

Abstract

1. 1. An in vivo model of the acute stage of gastric dilatation was prepared in fifty-seven rabbits under local anesthesia, with stomachs isolated from gastrointestinal continuity, but with intact blood supply and autonomic innervation. The roles of elevated transmural pressure and intraluminal acidity in the production of gastric injury were studied by observing bleeding rates, pathologic changes, and alterations in the net fluxes of H +, Na +, K +, and Cl - across the gastric mucosa. These changes were compared with those induced by acid and acetylsalicylic acid (ASA). 2. 2. The combination of ASA and acid within the lumen produced a small degree of bleeding and a pattern of widespread but superficial ulceration. Large increases in the net efflux of H + and Cl - from the lumen were associated with marked increases in Na + and K + influx. The concept of breakdown of the mucosal barrier to ionic diffusion in this form of injury is confirmed in the present study. 3. 3. High transmural pressure without intraluminal acidity produced a pathologic picture of subepithelial hemorrhage and edema without ulceration. A small but significant decrease in the net movement of Na + into the lumen was observed, but there were no significant changes in the net fluxes of the other ions measured. There was no appreciable bleeding into the lumen. 4. 4. The combination of intraluminal acidity and 30 cm. H 2O transmural pressure produced gross bleeding and deep, confluent, hemorrhagic ulcers, occasionally associated with transmural infarctions. A significantly increased efflux of H + from the lumen was observed in association with marginal changes in K + and Cl - fluxes. There was no detectable change in net Na + influx. A transmural pressure of 20 cm. H 2O in the presence of acid produced smaller changes of the same kind in the aforementioned parameters. None of the ion flux changes produced by pressure was as large as those observed in association with ASA. 5. 5. The changes produced by pressure alone indicate an injury to the gastric wall possibly due to local vascular compression, stasis, and anoxia. In the pressure of acid, the damaged mucosa may undergo ulceration, resulting in the fulminant “hemorrhagic gastritis” of acute gastric dilatation. The associated moderate ion flux changes are probably secondary phenomena. It is possible that the massive outpouring of fluid often seen after decompression of an acute gastric dilatation is secondary to this pressure-induced damage to the gastric wall.