title: Protein and fat utilization in shock.
abstract: A previous study demonstrated that in the dog, shock, regardless of its etiology, resulted in increased  oxidative utilization of substrates which form lactate and pyruvate as intermediary metabolites. The study implied a concomitant decrease in free fatty acid oxidation, as the oxidative pathway of the latter does not involve the lactate-pyruvate step. To test this hypothesis, free fatty acid metabolism was investigated by infusing carbon-14 labelled fatty acid in 12 normal dogs, in nine animals in shock due to controlled cardiac tamponade, and in six animals with endotoxin shock. The shock state was characterized by significant (p less than 0.05) decrease both in arterial fatty acid concentration and in free fatty acid turnover. In addition, both the rate of free fatty acid oxidation and the percentage of the total CO2 derived from free fatty acid oxidation were significantly (p less than 0.05) diminished. In contrast, urea production rates were higher in shock, and the calculated maximum contribution of protein oxidation to total CO2 production rose from 23% in the control animals to 50% in the test groups.
mesh_terms: D000818:Animals; D002210:Caprylates / Q000378:metabolism; D002245:Carbon Dioxide / Q000378:metabolism; D002305:Cardiac Tamponade / Q000150:complications; D004285:Dogs; D004731:Endotoxins; D004926:Escherichia coli; D005230:Fatty Acids, Nonesterified / Q000378:metabolism*; D005260:Female; D006801:Humans; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D011506:Proteins / Q000378:metabolism*; D012769:Shock / Q000209:etiology / Q000378:metabolism*; D012772:Shock, Septic / Q000378:metabolism; D014508:Urea / Q000096:biosynthesis
chemical_list: D002210:Caprylates; D004731:Endotoxins; D005230:Fatty Acids, Nonesterified; D011506:Proteins; D002245:Carbon Dioxide; D014508:Urea