It is shown that in patients with ulcer disease endogenous biosynthesis of prostaglandins E and F2~ in gastric and duodenal mucosa is suppressed. In patients treated with Venter (sucralfat), ulcer healing is accompanied by enhanced prostaglandin production in both scar tissue and unaffected areas. Stimulation of prostaglandin E and F2, " synthesis in the gastroduodenal mucosa followed by activation of their cytoprotective effect in the gastrointestinal system is a key mechanism underlying the effect of Venter.
The activity of adenylate cyclase in the hepatocyte plasma membranes, content of cAM P, and eAMP/cGMP ratio in the liver and blood plasma are decreased in patients with chronic liver diseases (fatty dystrophy, chronic hepatitis, and cirrhosis). This decrease depends on the disease severity and is most pronounced in cirrhosis. The sensitivity of liver adenylate cyclase to insulin and glucagon is changed. It is concluded that disorders in the adenylate cyclase system are an important molecular mechanism in the pathogenesis of chronic liver diseases.
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