• Arch Surg Chicago · Dec 1994

    Randomized Controlled Trial Comparative Study Clinical Trial

    Lipolysis in burned patients is stimulated by the beta 2-receptor for catecholamines.

    • D N Herndon, T T Nguyen, R R Wolfe, S P Maggi, G Biolo, M Muller, and R E Barrow.
    • Department of Surgery, University of Texas Medical Branch, Galveston.
    • Arch Surg Chicago. 1994 Dec 1; 129 (12): 1301-4; discussion 1304-5.

    ObjectiveTo determine if the cardiovascular effects of excessive catecholamines could be selectively blocked in severely burned patients without adversely affecting protein or fat kinetics.DesignProspective cohort study.SettingA large tertiary care referral center in Galveston, Tex.PatientsSixteen patients with greater than 40% body surface area burns.InterventionsPatients were randomly selected to receive propranolol hydrochloride, a nonselective beta 1- and beta 2-blocker, or metoprolol tartrate, a selective beta 1-blocker.Main Outcome MeasuresHeart rate; rate-pressure product; rate of appearance of urea, glucose, and leucine; and leucine oxidation were measured before and after selective or nonselective beta-adrenergic blockade.ResultsPropranolol and metoprolol caused a significant decrease in heart rate, from a mean (+/- SD) of 143 +/- 15 to 115 +/- 11 and from 147 +/- 17 to 120 +/- 9 beats per minute, respectively, during the 5-day study period. Neither the rate of appearance of urea nor the rate of urea production were significantly altered by propranolol or metoprolol therapy. Only propranolol produced a significant decrease (P < .05) in the rate of appearance of glycerol, from a mean (+/- SD) of 5.54 +/- 0.62 to 3.07 +/- 0.7 mumol/kg per minute. The rate of appearance of leucine, used as an index of total body protein catabolism, was not significantly altered by either beta-blocker.ConclusionsSelective beta 1-adrenergic blockade did not reduce lipolysis; however, a beta 1- and beta 2-adrenergic blockade significantly reduced lipolysis. Thus, the increased lipolysis, characteristic of severely burned patients, is caused by stimulation of the beta 2-adrenergic receptors for catecholamines.

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