Catecholamines: Mediator of the hypermetabolic response to thermal injury

D. W. Wilmore, J. M. Long, A. D. Mason, R. W. Skreen, B. A. Pruitt

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Abstract

Hypermetabolism characterizes the metabolic response to thermal injury and the extent of energy production is positively related to the rate of urinary catecholamine excretion. Alpha and beta adrenergic blockade decreased metabolism from 69.6 ± 5.3 Kcal/m2/hr to 57.4 ± 5.2 (P < 0.01), and infusion of 6 μgm epinephrine/min in normal man significantly increased metabolic rate. Twenty noninfected burned adults with a mean burn size of 45% total body surface (range 7-84%) and 4 normal controls were studied in an environmental chamber at 2 or more temperatures between 19 and 33 C with vapor pressure constant at 11.88 mm Hg. All burn patients were hypermetabolic at all temperatures studied and their core and mean skin temperatures were significantly elevated above control values. Between 25 and 33 C ambient, metabolism was unchanged in controls and burns of less than 40% total body surface (48.9 ± 4.6 Kcal/m2/hr vs. 48.9 ± 4.5), but metabolic rate decreased in larger burns in the warmer environment (72.0 ± 1.9 vs. 65.8 ± 1.7, p < 0.001). At 21 C, metabolism and catecholamines increased, except in 4 nonsurvivors who became hypothermic with decreased catechol elaboration. The metabolic rate in 10 patients with bacteremia was below predicted levels while catecholamines were markedly elevated suggesting interference with tissue uptake of the neurohormonal transmitters. Feeding burn patients or administering glucose and insulin improved nitrogen retention and altered substrate flow but did not significantly reduce urinary catecholamines or metabolic rate. Burned patients are internally warm, not externally cold, and catecholamines appear to mediate their increased heat production. Hypermetabolism may be modified by ambient temperature, infection, and pharmacologic means. Alterations in hypothalamic function due to injury, resulting in increased catecholamine elaboration, would explain the metabolic response to thermal injury.

Original languageEnglish (US)
Pages (from-to)653-669
Number of pages17
JournalUnknown Journal
Volume180
Issue number4
DOIs
StatePublished - Jan 1 1974

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ASJC Scopus subject areas

  • Surgery

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Wilmore, D. W., Long, J. M., Mason, A. D., Skreen, R. W., & Pruitt, B. A. (1974). Catecholamines: Mediator of the hypermetabolic response to thermal injury. Unknown Journal, 180(4), 653-669. https://doi.org/10.1097/00000658-197410000-00031