Pathophysiological mechanisms of adaptation of the mucosa of the gastric cardia to portal hypertension

Abstract

The model of before- and intrahepatic blockage of the portal system was proposed. Modeling of before-hepatic blockage of the portal system after development of toxic liver dystrophy lead to formation of the liver cirrhosis with stable portal hypertension. Gastritis with signs of hyperplastic and atrophy processes of the mucosa, formation of erosia, inflammatory infiltration of intermediate tissue and rebuilding of the glandulae were the basis of morphological changes of gastric mucosa in rats with experimental before- and intrahepatic portal blockage. Transformation of the cardiac mucosa with expressed polymorphism occured in the patients with the portal liver cirrhosis. Dystrophic and necrobiotic changes typical of hepatic gastropathy with signs of acute or chronic gastritis, formation of inflammatory infiltrates and rebuilding of the cardial mucosa into intestinal type were established microscopically. It is possible to believe that a widening of the veins leads to venous hyperemia and stasis in the portal hypertension. Therefore the morphology of the gastric mucosa was disturbed. It was accompanied bythe indurate changes and cellular destruction with erosia formation. These erosia may be a cause of rupture of the gastric mucosa in strong vomiting in Mallory-Weiss syndrome. This hypothesis needs clinic and experimental study in the future.