The relationship of burn-induced hypermetabolism to central and peripheral catecholamines.

The role of brain and circulating catecholamines as mediators of burn-induced hypermetabolism was investigated in two experiments. Following a 30% body surface area full-thickness open-flame burn, rats exhibited a short period (3 to 4 days) of anorexia followed by a more prolonged (several weeks) hyperphagic-hypermetabolic response. During this hypermetabolic period, norepinephrine concentrations were increased in the brain and circulating epinephrine levels were elevated. Depletion of brain norepinephrine using 6-hydroxydopamine led to increased body weight gain, but did not increase resting energy expenditure in burned rats. Similarly, the reduction of circulating catecholamines through removal of the adrenal medulla resulted in a decreased loss of body weight and only slight reductions in resting energy expenditure. Therefore, these results suggest that although brain norepinephrine and circulating epinephrine have a role in the full expression of hypermetabolism, these compounds do not appear to be major mediators of this response to burn trauma.