Portal hypertension predisposes the gastric mucosa to hemorrhagic shock/reperfusion injury.

We have previously demonstrated that the portal hypertensive (PHT) gastric mucosa has unique functional and morphologic features which predispose it to increased damage by noxious agents such as aspirin or alcohol. In this study we examine the PHT gastric mucosa following hemorrhagic shock and reperfusion. Portal hypertension was produced in 12 rats using staged portal vein occlusion, and seven animals (controls) underwent sham procedures. All rats received 2 ml 0.1 N HCl intragastrically. Shock was then induced by withdrawing blood to reduce systemic arterial pressures to approximately 30 mm Hg for 20 min. Blood was then reinfused and stomachs were excised 20 min later for gross and microscopic quantitation of injury. We found that gross damage to gastric glandular mucosa was more than doubled in PHT rats over sham-operated controls. In PHT gastric mucosa, deep histologic necrosis involved 22.5 +/- 3.8% of mucosal section lengths compared with 6.9 +/- 2.0% in control mucosa (P less than 0.005). Histologically, mucosal injury patterns were predominantly ischemic, with deep necrosis and disintegration of glands and microvessels, all prominently more extensive in PHT mucosa. We conclude that PHT gastric mucosa has significantly increased susceptibility to damage following hemorrhagic shock/reperfusion compared with portal normotensive mucosa. Since hemorrhagic shock is a frequent complication of portal hypertension, this study suggests clinical investigations of gastric mucosal function and pathophysiology in PHT patients following hemorrhage and resuscitation.