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Clinical Trial
. 1994 Dec;129(12):1301-4; discussion 1304-5.
doi: 10.1001/archsurg.1994.01420360091012.

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

Affiliations
Clinical Trial

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

D N Herndon et al. Arch Surg. 1994 Dec.

Abstract

Objective: To determine if the cardiovascular effects of excessive catecholamines could be selectively blocked in severely burned patients without adversely affecting protein or fat kinetics.

Design: Prospective cohort study.

Setting: A large tertiary care referral center in Galveston, Tex.

Patients: Sixteen patients with greater than 40% body surface area burns.

Interventions: Patients 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 measures: Heart 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.

Results: Propranolol 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.

Conclusions: Selective 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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