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

Abstract

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