Structural-metabolic aspects of the diagnosis of acute hepatic failure

et al. 1999

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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.

Section: Resultssupporting

confidence: 83%

Measurement of dehydrogenase activity in hepatocytes in massive pulmonary embolism

et al. 1999

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“…Since the liver is the central organ where detoxication occurs, disturbances in its structure and metabolism result in the development of liver and then multiple organ failure [10]. For a more Department reliable assessment of the morphofunctional changes and an explanation of the pathogenesis of the damage, the zonal structural-metabolic heterogeneity of hepatocytes in the acinus must be taken into consideration and correlation analysis must be used to study the interactions between the different metabolic pathways [7,9].…”

Section: Abstract: Liver Acinus; Metabolism; Peritonitis; Gangrenementioning

confidence: 99%

Comparative histophotometric characteristics of the structural-metabolic heterogeneity of hepatocytes in peritonitis and limb gangrene

1995

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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.

“…The main factor reliably indicating the threat of systemic pathological effects of endotoxemia is not so much the quantitative level of lipopolysaccharide in the bloodflow, but the failure of the organism's antitoxic defense systems and, primarily, of the liver [ 10]. The development of liver insufficiency is to a large extent determined by disorders of hepatocyte metabolism, the interzonal gradient of enzymatic activity in the liver acinus being one of its characteristics [4,5].This study was aimed at a histophotometric analysis of the activities of hepatocyte dehydrogenases in various acinus zones in the course of endotoxemia. …”

mentioning

confidence: 99%

Disorders in the structural and metabolic organization of liver acini in systemic endotoxemia

1995

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Injection of Escherichia coli lipopolysaccharide to dogs caused pronounced structural and metabolic changes of liver acini, characterized by the development of compensatory reactions to the endotoxin followed by their failure. In addition to hypoxia, depressed activity of hepatocyte dehydrogenases and diaphorases with impairment of the intraacinar gradient of their activity, leading to the development of hepatocellular insufficiency, appears to underlie the involvement of the liver in systemic endotoxemia. Key Words: liver acinus; metabolism; endotoxinPolyorgan insufficiency develops in the course of shock, and systemic endotoxemia of enteric origin plays an important role in its pathogenesis [7,17]. The main factor reliably indicating the threat of systemic pathological effects of endotoxemia is not so much the quantitative level of lipopolysaccharide in the bloodflow, but the failure of the organism's antitoxic defense systems and, primarily, of the liver [ 10]. The development of liver insufficiency is to a large extent determined by disorders of hepatocyte metabolism, the interzonal gradient of enzymatic activity in the liver acinus being one of its characteristics [4,5].This study was aimed at a histophotometric analysis of the activities of hepatocyte dehydrogenases in various acinus zones in the course of endotoxemia. MATERIALS AND METHODSThe study was carried out using 97 liver biopsy specimens from 11 mongrel dogs weighing 13 to 18 kg, intravenously infused Escherichia coli lipopolysaccharide in a single dose of 2 mg/kg. Oxygen tension in