A Program for Study of Skeletal Muscle Catabolism Following Physical Trauma.

To determine if the ketonemia following injury contributed to the increased glucogenesis associated with this catabolic disorder, glucose production and arterial substrates were measured before and after infusion of Na-DL-Beta-hydroxybutyrate beta-OHB, 20 Molkg.minute in fed, fasted, and fasted-infected sheep. Following three hours of beta-OHB infusion in the awake, conditioned animals, -OHB and acetoacetate blood concentrations more than doubled. With infusion, blood glucose and alanine concentrations decreased in the fed and fasted sheep but not in the fasted-infected group. Glucose production fell significantly. Glucose production was unaffected by beta-OHB infusion in the fasted-infected animals. The accelerated rate of glucose production in sheep following infection is not a consequence of the hypoketonemic state associated with sepsis. To determine the effect of the endorphine system on post-traumaticseptic metabolic responses, Naloxone 2 mg, I.V. was administered to four sheep, before and after infection. In these normotensive animals, no major alteration in substrate concentration was noted. The endorphine system does not appear to exert major metabolic regulatory effects in this model.