Comparative histophotometric and correlation analysis was carried out to study dehydrogenase activity in hepatocytes of different acinar zones in peritonitis and gangrene of the lower extremities. Structural-metabolic disturbances of hepatocytes were found to be responsible for the weakened detoxicating function in patients with endotoxicoses. Special features of metabolic disturbances in the liver acini were demonstrated in peritonitis and limb gangrene.

A histophotometric study of the liver dehydrogenase activity reveals the nature of changes of enzymatic homeostasis and its periodicity in the dynamics of endotoxinemia in dogs. A compensatory reaction to lipopolysaccharide administration develops during the first two hours. A decrease of dehydrogenase and diaphorase activity and the development of structural damage to hepatocytes appear later. It is shown that the activation of free-radical oxidation as well as an increase of the level of medium-sized molecules in the blood plasma play a key role in the pathogenesis of liver damage.

Experimental massive pulmonary embolism in dogs induces structural and metabolic changes in the liver. The severity of these changes depends on the duration of the postembolization period and the development of heart failure. Key Words: hepatocyte; dehydrogenases," pulmonaJT embolismMassive pulmonary embolism (MPE) poses a real threat for patient's life due to the development of acute cardiovascular insufficiency. In light of this, changes in the heart and pulmonary vessels are extensively studied [2,7,9]. However, other organs are also altered in MPE, in particular, liver dysfunction plays an important role in the pathogenesis of postembolization syndrome.The aim of the present study was to evaluate structural and metabolic changes in dog liver in MPE accompanied and not accompanied by heart failure. MATERIALS AND METHODSExperiments were carried out on 37 mature mongrel dogs weighing 18-20 kg. The animals were fed standard vivarium chow and received no chow 12 h before study. The experiments were carried on closed chest and under conditions of natural respiration. The animals were narcotized with sodium thiopental (20 mg/kg, intravenously) after promedol premedication (10 mg/ kg). Longitudinal fragments of canine sartorial muscle were used for embolization. MPE modeling and catheterization of the heart and vessels were described previously [1]. Heart rate (HR), ECG, respiration rate, and blood pressure in the aorta were recorded. The animals were divided into 4 groups: compensated MPE for 1 and 6 h (MPE without heart failure, euthanasia) and uncompensated MPE for 1 and 6 h (death from cardiovascular insufficiency within 1 and 6 h after MPE modeling). In two control groups the animals were immobilized and narcotized after premedication, the heart and vessels were catheterized, and the animals were euthanized after 1 and 6 h by sodium thiopental overdose.Liver samples were frozen and stored in liquid nitrogen. On parallel cryostat sections, activities of succinate dehydrogenase (SDH), 3-hydroxybutyrate dehydrogenase (BDH), glucose-6-phosphate dehydrogenase (G6PD), lactate dehydrogenase (LDH), and NADH and NADPH diaphorases were histochemically assayed [4]. Enzyme activities were evaluated using a Microvideomat TV image analysis system (Opton). Paraffin sections were stained with hematoxylin and eosin. The data were processed statistically.