Persistent gastric mucosal hypoxia and interstitial edema after hemorrhagic shock: prevention with steroid therapy.

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 hours 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 minutes 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 minutes 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 dialted capillaries in the lamina propria; methylprednisolone treatment prevented these changes. We conclude that pathophysiological arteriovenous shunting occurs in the microcirculation of the apical faveoli and speculate that 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. These findings suggest an explanation for the paradox between restoration of mucosal blood flow and continued mucosal injury which occur after shock.