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Profound hepatic tissue morphofunctional changes with progressive hepatic failure occur in endotoxicosis caused by peritonitis and lower extremity gangrene. Comparative quantitative histoenzymatic and biochemical studies have revealed hepatic metabolic disturbances in peritonitis and leg gangrene.

The indices of portal bacteremia and endotoxinemia, parameters of metabolism, hepatic hemodynamics, the phagocytic function of the liver and leukocyte reaction were studied in 13 patients with diffuse peritonitis of different etiology. Close interconnections of the level of portal toxemia is shown with the degree of activation of the phagocytic function of the liver, changes in hepatic hemodynamics, degree of metabolic disturbances playing an important role in pathogenesis of polyorganic insufficiency as well as the role of leukocytic reaction in microendocrinous regulation of metabolism in peritonitis.

In 48 patients operated on for peritonitis of different etiology the postoperative period was complicated by the onset of adult respiratory distress syndrome. A considerable increase in the blood level of biologically active compounds (adrenalin, noradrenalin, histamine, serotonin) and the activation of kinin system have been observed. Marked humoral shifts trigger a sequence of reactions manifested in microcirculation disturbances and the onset of tissue hypoxia, thus inducing the damage of metabolic lung functions and the development of adult respiratory distress syndrome.

Systemic and hepatic hemodynamics, gas exchange, acid-base balance in blood from the artery, portal, hepatic and peripheral veins were examined in 113 patients with diffuse peritonitis varying etiologically. In view of adequate tissue perfusion and oxygen transport revealed it is suggested that causes of metabolic derangement arising in peritonitis and responsible for multiple organ insufficiency should be searched into at the level of intracellular metabolism.