ROLE OF TISSUE PLASMINOGEN ACTIVATOR AND LYSOSOMAL ENZYME IN EXPERIMNTAL PROTEIN-LOSING GASTROPAHTY

Abstract

Role of tissue fibrinolysis in the pathogenesis of protein-losing gastropathy was further investigated in an experimental model of dogs using Dithiothreitol (DTT).
Perfusion of the dog stomach revealed increased protein loss from the gastric mucosa in association with the elevation of either fibrinolytic activity or β-glucuronidase activity in the biopsied gastric mucosa. Beta-glucuronidase activity was also found to increase in the gastric perfusate in the presence of DTT. Antifibrinolytic agent, trans-AMCHA, revealed suppressive effect on protein loss into the gastric cavity induced by DTT, while failed to reduce β-glucoronidase activity in the gastric mucosa.
It was concluded that tissue fibrinolytic activity in the gastric mucosa was increased by the use of DTT, and to which lysosomal labilization seemen to play a part. Trans-AMCHA acted as an inhibitor of fibrinolytic system, and probably not as a stabilizer of lysosomal enzyme, and exerted the preventing effect on the protein loss through the gastric mucosa.