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Lipolysis in Burned Patients Is Stimulated by the β2-Receptor for Catecholamines

Lipolysis in Burned Patients Is Stimulated by the β2-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. 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 β1- and β2-blocker, or metoprolol tartrate, a selective β1-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 β-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 μmol/kg per minute. The rate of appearance of leucine, used as an index of total body protein catabolism, was not significantly altered by either β-blocker. Conclusions: Selective β1-adrenergic blockade did not reduce lipolysis; however, a β1- and β2-adrenergic blockade significantly reduced lipolysis. Thus, the increased lipolysis, characteristic of severely burned patients, is caused by stimulation of the β2-adrenergic receptors for catecholamines.(Arch Surg. 1994;129:1301-1305) References 1. Wilmore DW, Long JM, Mason AD Jr, Robert W, Skreen BS, Pruitt BA Jr. Catecholamines: mediator of the hypermetabolic response to thermal injury . Ann Surg . 1974:180:653-668.Crossref 2. Arturson G. Prostaglandins in human burn wound secretions . Burns . 1977:3: 112-118.Crossref 3. Goodal MC, Stone C, Haynes BW Jr. Urinary output of adrenaline and nonadrenaline in severe thermal injuries . Ann Surg . 1957;145:479-487.Crossref 4. Wolfe RR, Herndon DN, Peters EJ, Jahoor F, Desai MH, Holland OB. Regulation of lipolysis in severely burned children . Ann Surg . 1987;290:214-221.Crossref 5. Herndon DN, Curreri PW, Abston S, Rutan TC, Barrow RE. Treatment of burns . In: Ravitch MM, ed. Current Problems in Surgery . Chicago, III: Mosby-Year Book Medical Publishers; 1987:341-397. 6. Herndon DN, Stein ND, Rutan TC, Abston S, Linares H. Failure of TPN supplementation to improve liver function, immunity and mortality in thermally injured patients . J Trauma . 1987;27:195-204.Crossref 7. Linares HA. A report of 115 consecutive autopsies in burned children, 1966-1980 . Burns . 1982;8:263-270.Crossref 8. Joshi VV. Effects of burns on the heart . JAMA . 1970;211:2130-2134.Crossref 9. Gelfand RA, Hutchinson-Williams KA, Bonde AA, Castellino P, Sherwin RS. Catabolic effects of thyroid hormone excess: the contribution of adrenergic activity to hypermetabolism and protein breakdown . Metabolism . 1987;36:562-569.Crossref 10. Herndon DN, Barrow RE, Rutan TC, Minifee P, Jahoor R, Wolfe RR. Effect of propranolol administration on hemodynamic and metabolic responses of burned pediatric patients . Ann Surg . 1988;208:484-492.Crossref 11. Garber AJ, Karl IE, Kipnis DM. Alanine and glutamine synthesis and release from skeletal muscle, IV: β-adrenergic inhibition of amino acid release . J Biol Chem . 1976;251:851-857. 12. Miles JM, Nissen SL, Gerich JE, Haymond MW. Effects of epinephrine infusion on leucine and alanine kinetics in humans . Am J Physiol . 1984;247:E166-E172. 13. Keller U, Kraenzlin W, Stauffacher W, Arnaud M. β-adrenergic stimulation results in diminished protein breakdown, decreased amino acid oxidation and increased protein synthesis in man . JPEN J Parenter Enteral Nutr . 1987;11: 7S. Abstract 29. 14. Wolfe RR. Tracer in Metabolic Research: Radioisotope and Stable Isotope/Mass Spectrometry Methods. New York, NY: Alan R Liss Inc; 1984:261-263. 15. Wolfe RR, Durkot MJ. Evaluation of the role of the sympathetic nervous system in the response of substrate kinetics and oxidation to burn injury . Circ Shock . 1982;9:395-406. 16. Layman DL, Wolfe RR. Sample site selection for tracer studies applying a unidirectional circulatory approach . Am J Physiol . 1987;253:E173-E178. 17. Schenk WF, Beaufrere B, Haymond MW. Use of reciprocal pool activities to model leucine metabolism in man following bedrest . Am J Physiol . 1988;255: E548-E558. 18. Allsop JR, Wolfe RR, Burke JF. Tracer priming the bicarbonate pool . J Appl Physiol . 1978;45:137-139. 19. Harris JA, Benedict FG. A Biometric Study of Basal Metabolism in Man. Washington, DC: Carnegie Institute of Washington; 1919:40-44. Publication 297. 20. Harrison TS, Seaton JF, Feller AB. Relationship of increased oxygen consumption to catecholamine excretion in thermal burns . Ann Surg . 1967;165:169-172.Crossref 21. Harrison TS. In discussion: Wilmore DW, Long JM, Mason AD Jr, Robert W, Skreen BS, Pruitt BA Jr. Catecholamines: mediators of the hypermetabolic response to thermal injury . Ann Surg . 1974;180:668-669. 22. Raab W. Key position of catecholamines in functional and degenerative cardiovascular pathology . Am J Cardiol . 1960;5:571-578.Crossref 23. Gobel FL, Nordstrom LA, Nelson RR, Jorgensen CR, Wang Y. The ratepressure product as an index of myocardial oxygen consumption during exercise in patients with angina pectoris . Circulation . 1978;57:549-556.Crossref 24. Baller D, Bretschneider HJ, Hellige G. Validity of myocardial oxygen consumption parameters . Clin Cardiol . 1979;2:317-327.Crossref 25. Baller D, Bretschneider JH, Hellige G. A critical look at currently used indirect indices of myocardial oxygen consumption . Basic Res Cardiol . 1981;76:163-181.Crossref 26. Wolfe RR, Herndon DN, Jahoor F, Miyoshi H, Wolfe M. Effects of severe burn injury on substrate cycling by glucose and fatty acids . N Engl J Med . 1987; 317:403-408.Crossref 27. Hellerstein MK, Christiansen M, Kaempfer S, et al. Measurement of de novo hepatic lipogenesis in humans using stable isotopes . JClin Invest . 1991;87: 1841-1852.Crossref 28. Wolfe RR, Goodenough RD, Wolfe M, Royle GT, Nadel ER. Isotopic analysis of leucine and urea metabolism in exercising humans . J Appl Physiol . 1982; 52:458-466. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Surgery American Medical Association

Lipolysis in Burned Patients Is Stimulated by the β2-Receptor for Catecholamines

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Publisher
American Medical Association
Copyright
Copyright © 1994 American Medical Association. All Rights Reserved.
ISSN
0004-0010
eISSN
1538-3644
DOI
10.1001/archsurg.1994.01420360091012
Publisher site
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Abstract

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 β1- and β2-blocker, or metoprolol tartrate, a selective β1-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 β-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 μmol/kg per minute. The rate of appearance of leucine, used as an index of total body protein catabolism, was not significantly altered by either β-blocker. Conclusions: Selective β1-adrenergic blockade did not reduce lipolysis; however, a β1- and β2-adrenergic blockade significantly reduced lipolysis. Thus, the increased lipolysis, characteristic of severely burned patients, is caused by stimulation of the β2-adrenergic receptors for catecholamines.(Arch Surg. 1994;129:1301-1305) References 1. Wilmore DW, Long JM, Mason AD Jr, Robert W, Skreen BS, Pruitt BA Jr. Catecholamines: mediator of the hypermetabolic response to thermal injury . Ann Surg . 1974:180:653-668.Crossref 2. Arturson G. Prostaglandins in human burn wound secretions . Burns . 1977:3: 112-118.Crossref 3. Goodal MC, Stone C, Haynes BW Jr. Urinary output of adrenaline and nonadrenaline in severe thermal injuries . Ann Surg . 1957;145:479-487.Crossref 4. Wolfe RR, Herndon DN, Peters EJ, Jahoor F, Desai MH, Holland OB. Regulation of lipolysis in severely burned children . Ann Surg . 1987;290:214-221.Crossref 5. Herndon DN, Curreri PW, Abston S, Rutan TC, Barrow RE. Treatment of burns . In: Ravitch MM, ed. Current Problems in Surgery . Chicago, III: Mosby-Year Book Medical Publishers; 1987:341-397. 6. Herndon DN, Stein ND, Rutan TC, Abston S, Linares H. Failure of TPN supplementation to improve liver function, immunity and mortality in thermally injured patients . J Trauma . 1987;27:195-204.Crossref 7. Linares HA. A report of 115 consecutive autopsies in burned children, 1966-1980 . Burns . 1982;8:263-270.Crossref 8. Joshi VV. Effects of burns on the heart . JAMA . 1970;211:2130-2134.Crossref 9. Gelfand RA, Hutchinson-Williams KA, Bonde AA, Castellino P, Sherwin RS. Catabolic effects of thyroid hormone excess: the contribution of adrenergic activity to hypermetabolism and protein breakdown . Metabolism . 1987;36:562-569.Crossref 10. Herndon DN, Barrow RE, Rutan TC, Minifee P, Jahoor R, Wolfe RR. Effect of propranolol administration on hemodynamic and metabolic responses of burned pediatric patients . Ann Surg . 1988;208:484-492.Crossref 11. Garber AJ, Karl IE, Kipnis DM. Alanine and glutamine synthesis and release from skeletal muscle, IV: β-adrenergic inhibition of amino acid release . J Biol Chem . 1976;251:851-857. 12. Miles JM, Nissen SL, Gerich JE, Haymond MW. Effects of epinephrine infusion on leucine and alanine kinetics in humans . Am J Physiol . 1984;247:E166-E172. 13. Keller U, Kraenzlin W, Stauffacher W, Arnaud M. β-adrenergic stimulation results in diminished protein breakdown, decreased amino acid oxidation and increased protein synthesis in man . JPEN J Parenter Enteral Nutr . 1987;11: 7S. Abstract 29. 14. Wolfe RR. Tracer in Metabolic Research: Radioisotope and Stable Isotope/Mass Spectrometry Methods. New York, NY: Alan R Liss Inc; 1984:261-263. 15. Wolfe RR, Durkot MJ. Evaluation of the role of the sympathetic nervous system in the response of substrate kinetics and oxidation to burn injury . Circ Shock . 1982;9:395-406. 16. Layman DL, Wolfe RR. Sample site selection for tracer studies applying a unidirectional circulatory approach . Am J Physiol . 1987;253:E173-E178. 17. Schenk WF, Beaufrere B, Haymond MW. Use of reciprocal pool activities to model leucine metabolism in man following bedrest . Am J Physiol . 1988;255: E548-E558. 18. Allsop JR, Wolfe RR, Burke JF. Tracer priming the bicarbonate pool . J Appl Physiol . 1978;45:137-139. 19. Harris JA, Benedict FG. A Biometric Study of Basal Metabolism in Man. Washington, DC: Carnegie Institute of Washington; 1919:40-44. Publication 297. 20. Harrison TS, Seaton JF, Feller AB. Relationship of increased oxygen consumption to catecholamine excretion in thermal burns . Ann Surg . 1967;165:169-172.Crossref 21. Harrison TS. In discussion: Wilmore DW, Long JM, Mason AD Jr, Robert W, Skreen BS, Pruitt BA Jr. Catecholamines: mediators of the hypermetabolic response to thermal injury . Ann Surg . 1974;180:668-669. 22. Raab W. Key position of catecholamines in functional and degenerative cardiovascular pathology . Am J Cardiol . 1960;5:571-578.Crossref 23. Gobel FL, Nordstrom LA, Nelson RR, Jorgensen CR, Wang Y. The ratepressure product as an index of myocardial oxygen consumption during exercise in patients with angina pectoris . Circulation . 1978;57:549-556.Crossref 24. Baller D, Bretschneider HJ, Hellige G. Validity of myocardial oxygen consumption parameters . Clin Cardiol . 1979;2:317-327.Crossref 25. Baller D, Bretschneider JH, Hellige G. A critical look at currently used indirect indices of myocardial oxygen consumption . Basic Res Cardiol . 1981;76:163-181.Crossref 26. Wolfe RR, Herndon DN, Jahoor F, Miyoshi H, Wolfe M. Effects of severe burn injury on substrate cycling by glucose and fatty acids . N Engl J Med . 1987; 317:403-408.Crossref 27. Hellerstein MK, Christiansen M, Kaempfer S, et al. Measurement of de novo hepatic lipogenesis in humans using stable isotopes . JClin Invest . 1991;87: 1841-1852.Crossref 28. Wolfe RR, Goodenough RD, Wolfe M, Royle GT, Nadel ER. Isotopic analysis of leucine and urea metabolism in exercising humans . J Appl Physiol . 1982; 52:458-466.

Journal

Archives of SurgeryAmerican Medical Association

Published: Dec 1, 1994

References