Inhibition of catecholamine-induced calorigenesis and lipolysis by hypercapnic acidosis

Abstract

The calorigenic and metabolic effects of norepinephrine (NE) and epinephrine (E) (1.5 [mu]g/kg/min. for 30 min.) were studied in 8 young, healthy beagles, mechanically ventilated at normal pH and during hypercapnic acidosis (pH =,7.0, PCO2 = 90 mm Hg). Both NE and E increased O2 consumption (VO2) to the same extent (25-30%) at normal pH. During hypercapnic acidosis this calorigenic effect of E and NE was inhibited, no significant changes in VO2 occurring. Hyperglycemic responses to catecholamine infusion were not changed by acidosis. The rise of plasma FFA [free fatty acid] observed at normal pH after catecholamine infusion was inhibited by acidosis. During E infusion blood glycerol increased at normal pH; this increase was markedly reduced at low pH. These data indicate that catecholamine-induced calorigenesis and lipolysis are inhibited by hypercapnic acidosis. In addition, similar studies were performed in 6 animals during and after similar exposure to hypercapnic acidosis which stimulates the release of endogenous catecholamines. During acidosis, VO2, FFA, and glycerol did not change significantly, whereas glucose increased. When pH was restored to normal, VO2, FFA, and glycerol increased, while glucose remained elevated. These data indicate that an increase in [H+] exerts antagonistic effects on catecholamines, on the one hand stimulating their release but, on the other hand, inhibiting their metabolic effects.