title: Lipolysis in burned patients is stimulated by the beta 2-receptor for catecholamines.
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.
  
  
  METHODS
  Prospective cohort study.
  
  
  METHODS
  A large tertiary care referral center in Galveston, Tex.
  
  
  METHODS
  Sixteen patients with greater than 40% body surface area burns.
  
  
  METHODS
  Patients were randomly selected to receive propranolol hydrochloride, a nonselective beta 1- and beta 2-blocker, or metoprolol tartrate, a selective beta 1-blocker.
  
  
  METHODS
  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.
authors.affiliation: Department of Surgery, University of Texas Medical Branch, Galveston.
authors.forename: D N
authors.initials: DN
authors.lastname: Herndon
authors.forename: T T
authors.initials: TT
authors.lastname: Nguyen
authors.forename: R R
authors.initials: RR
authors.lastname: Wolfe
authors.forename: S P
authors.initials: SP
authors.lastname: Maggi
authors.forename: G
authors.initials: G
authors.lastname: Biolo
authors.forename: M
authors.initials: M
authors.lastname: Muller
authors.forename: R E
authors.initials: RE
authors.lastname: Barrow
mesh_terms: D000293:Adolescent; D000328:Adult; D001806:Blood Urea Nitrogen; D001830:Body Surface Area; D002056:Burns / Q000145:classification / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology; D005990:Glycerol / Q000097:blood; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007930:Leucine / Q000097:blood; D008066:Lipolysis / Q000187:drug effects*; D008790:Metoprolol / Q000494:pharmacology*; D011433:Propranolol / Q000494:pharmacology*; D011446:Prospective Studies; D018343:Receptors, Adrenergic, beta-2 / Q000187:drug effects*
chemical_list: D018343:Receptors, Adrenergic, beta-2; D011433:Propranolol; D008790:Metoprolol; D007930:Leucine; D005990:Glycerol