ROLE OF STRESS HORMONES IN THE CATABOLIC METABOLISM OF SHOCK

Abstract

The role of catecholamines in shock metabolism in dogs was studied by comparing the metabolism of shock due to cardiac tamponade, shock with catecholamine depletion from prior reserpine administration and metabolism in the normal dog with continuous epinephrine infusion. The high serum concentrations of catecholamines in shock probably cause the increased blood lactate, initial hyperglycemia and, possibly, the poor free fatty acid [FFA] oxidation seen in shock, but do not cause the increased protein catabolism of shock. With the simultaneous infusion of glucagon, cortisol and epinephrine in physiologic dosages, catabolic metabolism similar to that observed in shock was established in the normal dog. Lactacidemia, hyperglycemia, poor ability to oxidize FFA and massive protein breakdown were observed. The decreased metabolic rate and diminished fatty acid mobilization of shock were not duplicated in those in the normal group and are probably a function of hypoperfusion. Impaired use of fat and increased protein breakdown, as seen in shock and trauma, are mediated by hormonal changes. It follows that there may be the opportunity to reverse or modify this catabolism by hormonal manipulation in the surgical patient.