PERSISTENT GASTRIC MUCOSAL HYPOXIA AND INTERSTITIAL EDEMA AFTER HEMORRHAGIC-SHOCK - PREVENTION WITH STEROID-THERAPY

Abstract

To define the role of the nutrient microvasculature in the pathogenesis of acute gastric mucosal erosions, a correlation was performed of changes in intracellular oxygenation (ICPO2) and intracellular potential difference (ICPD) in surface epithelial cells with the histological alterations in the apices of the faveoli of canine gastric mucosa after 3 h of hemorrhagic shock. ICPO2 fell from 16.7 .+-. 0.8 mm Hg before shock to 5.4 .+-. 0.9 mm Hg at the end of shock. Ninety min after reinfusion of blood and restoration of total gastric blood flow to baseline levels, ICPO2 was 5.8 .+-. 0.7 mm Hg. ICPD changes were similar, but more gradual. Treatment with methylprednisolone (30 mg/kg) 30 min after hemorrhage ameliorated mucosal hypoxia during shock (10.9 .+-. 1.0 mm Hg) and prevented it after resuscitation (15.4 .+-. 0.8 mm Hg). The microscopic anatomy of untreated gastric mucosae showed severe subepithelial edema with dilated capillaries in the lamina propria. Methylprednisolone treatment prevented these changes. Pathophysiological arteriovenous shunting occurs in the microcirculation of the apical faveoli. It is caused either by redistribution of nutrient blood flow away from the surface epithelium or by increased permeability of the microvascular endothelium with concomitant mucosal interstitial edema. An explanation may exist for the paradox between restoration of mucosal blood flow and continued mucosal injury which occur after shock.