Pulmonary cellular dysfunction in endotoxin shock: metabolic and transport derangements.
Lung cell metabolic and ion transport alterations in endotoxin shock have been studied to elucidate mechanisms of endotoxin-induced pulmonary dysfunction. Glucose oxidation to lactate as well as to CO2 is significantly increased with a decrease in the lung ATP contents. Active Na+ transport is impaired, indicating an increase in lung intracellular fluid. The altered glucose metabolism and active ion transport could potentially contribute to lung edemagenesis in endotoxicosis.
D000227:Adenine Nucleotides / Q000096:biosynthesis; D000255:Adenosine Triphosphate / Q000378:metabolism; D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D001692:Biological Transport; D002199:Capillary Permeability / Q000187:drug effects; D000242:Cyclic AMP / Q000378:metabolism; D004731:Endotoxins / Q000494:pharmacology; D006168:Guinea Pigs; D007424:Intracellular Fluid / Q000378:metabolism; D007773:Lactates / Q000096:biosynthesis; D019344:Lactic Acid; D008168:Lung / Q000378:metabolism*; D008297:Male; D012770:Shock, Cardiogenic / Q000378:metabolism*
D000227:Adenine Nucleotides; D004731:Endotoxins; D007773:Lactates; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D000242:Cyclic AMP; D000262:Adenylyl Cyclases