β-adrenergic desensitization after burn excision not affected by the use of epinephrine to limit blood loss

Christopher McQuitty, Jeffrey Berman, Joaquin Cortiella, David Herndon, Mali Mathru

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Background: Burn patients have impaired myocardial function and decreased β-adrenergic responsiveness. Further β-adrenergic dysfunction from systemic absorption of topically administered epinephrine that is given to limit blood loss during burn excision could affect perioperative management. The authors evaluated the effect of topical epinephrine administration to patients during burn excision on the lymphocytic β-adrenergic response. Methods: Fifty-five patients (age, 2-18 yr) with 20-90% body surface area burns received a standardized anesthetic for a burn excision procedure. Lymphocyte samples were taken at baseline and 1 and 3 h after the initial use of epinephrine (n = 43) or thrombin (controls, n = 12). Plasma epinephrine levels were measured by high-performance liquid chromatography. Lymphocyte β-adrenergic responsiveness was assessed by measuring production of cyclic adenosine monophosphate (cAMP) after stimulation with isoproterenol, prostaglandin E 1 (PGE 1), and forskolin. β-adrenergic receptor binding assays using iodopindolol and CGP12177 yielded β-adrenergic receptor density. Results: Epinephrine levels were elevated at 1 h (P < 0.01) and 3 h (P < 0.01) after epinephrine use but not in control patients. Production of cAMP in lymphocytes 1 h after epinephrine was greater in patients receiving epinephrine than in control patients on stimulation with isoproterenol (P < 0.05) and PGE 1 (P < 0.05). Three hours after epinephrine administration, production of cAMP decreased when compared with baseline in both control patients and those receiving epinephrine after stimulation with isoproterenol (P < 0.05), PGE 1 (P < 0.05), and forskolin (P < 0.05). Lymphocytic β-adrenergic receptor content was not changed. Conclusions: Topical epinephrine to limit blood loss during burn excision resulted in significant systemic absorption and increased plasma epinephrine levels. Acute sensitization of the lymphocytic β-adrenergic cascade was induced by the administration of epinephrine reflected by increased cAMP production after stimulation with isoproterenol and PGE 1. The lymphocytic β-adrenergic cascade exhibited homologous and heterologous desensitization 3 h after the use of epinephrine or thrombin, indicating that epinephrine administration was not a causative factor.

Original languageEnglish (US)
Pages (from-to)351-358
Number of pages8
JournalAnesthesiology
Volume93
Issue number2
StatePublished - 2000

Fingerprint

Adrenergic Agents
Epinephrine
Prostaglandins E
Isoproterenol
Cyclic AMP
Adrenergic Receptors
Colforsin
Lymphocytes
Thrombin
Topical Administration
Body Surface Area
Burns
Anesthetics
High Pressure Liquid Chromatography

Keywords

  • Catecholamines
  • Pediatrics
  • Receptors

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

β-adrenergic desensitization after burn excision not affected by the use of epinephrine to limit blood loss. / McQuitty, Christopher; Berman, Jeffrey; Cortiella, Joaquin; Herndon, David; Mathru, Mali.

In: Anesthesiology, Vol. 93, No. 2, 2000, p. 351-358.

Research output: Contribution to journalArticle

@article{9fbfd6ea33bb463fbff31c6e492d5581,
title = "β-adrenergic desensitization after burn excision not affected by the use of epinephrine to limit blood loss",
abstract = "Background: Burn patients have impaired myocardial function and decreased β-adrenergic responsiveness. Further β-adrenergic dysfunction from systemic absorption of topically administered epinephrine that is given to limit blood loss during burn excision could affect perioperative management. The authors evaluated the effect of topical epinephrine administration to patients during burn excision on the lymphocytic β-adrenergic response. Methods: Fifty-five patients (age, 2-18 yr) with 20-90{\%} body surface area burns received a standardized anesthetic for a burn excision procedure. Lymphocyte samples were taken at baseline and 1 and 3 h after the initial use of epinephrine (n = 43) or thrombin (controls, n = 12). Plasma epinephrine levels were measured by high-performance liquid chromatography. Lymphocyte β-adrenergic responsiveness was assessed by measuring production of cyclic adenosine monophosphate (cAMP) after stimulation with isoproterenol, prostaglandin E 1 (PGE 1), and forskolin. β-adrenergic receptor binding assays using iodopindolol and CGP12177 yielded β-adrenergic receptor density. Results: Epinephrine levels were elevated at 1 h (P < 0.01) and 3 h (P < 0.01) after epinephrine use but not in control patients. Production of cAMP in lymphocytes 1 h after epinephrine was greater in patients receiving epinephrine than in control patients on stimulation with isoproterenol (P < 0.05) and PGE 1 (P < 0.05). Three hours after epinephrine administration, production of cAMP decreased when compared with baseline in both control patients and those receiving epinephrine after stimulation with isoproterenol (P < 0.05), PGE 1 (P < 0.05), and forskolin (P < 0.05). Lymphocytic β-adrenergic receptor content was not changed. Conclusions: Topical epinephrine to limit blood loss during burn excision resulted in significant systemic absorption and increased plasma epinephrine levels. Acute sensitization of the lymphocytic β-adrenergic cascade was induced by the administration of epinephrine reflected by increased cAMP production after stimulation with isoproterenol and PGE 1. The lymphocytic β-adrenergic cascade exhibited homologous and heterologous desensitization 3 h after the use of epinephrine or thrombin, indicating that epinephrine administration was not a causative factor.",
keywords = "Catecholamines, Pediatrics, Receptors",
author = "Christopher McQuitty and Jeffrey Berman and Joaquin Cortiella and David Herndon and Mali Mathru",
year = "2000",
language = "English (US)",
volume = "93",
pages = "351--358",
journal = "Anesthesiology",
issn = "0003-3022",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - β-adrenergic desensitization after burn excision not affected by the use of epinephrine to limit blood loss

AU - McQuitty, Christopher

AU - Berman, Jeffrey

AU - Cortiella, Joaquin

AU - Herndon, David

AU - Mathru, Mali

PY - 2000

Y1 - 2000

N2 - Background: Burn patients have impaired myocardial function and decreased β-adrenergic responsiveness. Further β-adrenergic dysfunction from systemic absorption of topically administered epinephrine that is given to limit blood loss during burn excision could affect perioperative management. The authors evaluated the effect of topical epinephrine administration to patients during burn excision on the lymphocytic β-adrenergic response. Methods: Fifty-five patients (age, 2-18 yr) with 20-90% body surface area burns received a standardized anesthetic for a burn excision procedure. Lymphocyte samples were taken at baseline and 1 and 3 h after the initial use of epinephrine (n = 43) or thrombin (controls, n = 12). Plasma epinephrine levels were measured by high-performance liquid chromatography. Lymphocyte β-adrenergic responsiveness was assessed by measuring production of cyclic adenosine monophosphate (cAMP) after stimulation with isoproterenol, prostaglandin E 1 (PGE 1), and forskolin. β-adrenergic receptor binding assays using iodopindolol and CGP12177 yielded β-adrenergic receptor density. Results: Epinephrine levels were elevated at 1 h (P < 0.01) and 3 h (P < 0.01) after epinephrine use but not in control patients. Production of cAMP in lymphocytes 1 h after epinephrine was greater in patients receiving epinephrine than in control patients on stimulation with isoproterenol (P < 0.05) and PGE 1 (P < 0.05). Three hours after epinephrine administration, production of cAMP decreased when compared with baseline in both control patients and those receiving epinephrine after stimulation with isoproterenol (P < 0.05), PGE 1 (P < 0.05), and forskolin (P < 0.05). Lymphocytic β-adrenergic receptor content was not changed. Conclusions: Topical epinephrine to limit blood loss during burn excision resulted in significant systemic absorption and increased plasma epinephrine levels. Acute sensitization of the lymphocytic β-adrenergic cascade was induced by the administration of epinephrine reflected by increased cAMP production after stimulation with isoproterenol and PGE 1. The lymphocytic β-adrenergic cascade exhibited homologous and heterologous desensitization 3 h after the use of epinephrine or thrombin, indicating that epinephrine administration was not a causative factor.

AB - Background: Burn patients have impaired myocardial function and decreased β-adrenergic responsiveness. Further β-adrenergic dysfunction from systemic absorption of topically administered epinephrine that is given to limit blood loss during burn excision could affect perioperative management. The authors evaluated the effect of topical epinephrine administration to patients during burn excision on the lymphocytic β-adrenergic response. Methods: Fifty-five patients (age, 2-18 yr) with 20-90% body surface area burns received a standardized anesthetic for a burn excision procedure. Lymphocyte samples were taken at baseline and 1 and 3 h after the initial use of epinephrine (n = 43) or thrombin (controls, n = 12). Plasma epinephrine levels were measured by high-performance liquid chromatography. Lymphocyte β-adrenergic responsiveness was assessed by measuring production of cyclic adenosine monophosphate (cAMP) after stimulation with isoproterenol, prostaglandin E 1 (PGE 1), and forskolin. β-adrenergic receptor binding assays using iodopindolol and CGP12177 yielded β-adrenergic receptor density. Results: Epinephrine levels were elevated at 1 h (P < 0.01) and 3 h (P < 0.01) after epinephrine use but not in control patients. Production of cAMP in lymphocytes 1 h after epinephrine was greater in patients receiving epinephrine than in control patients on stimulation with isoproterenol (P < 0.05) and PGE 1 (P < 0.05). Three hours after epinephrine administration, production of cAMP decreased when compared with baseline in both control patients and those receiving epinephrine after stimulation with isoproterenol (P < 0.05), PGE 1 (P < 0.05), and forskolin (P < 0.05). Lymphocytic β-adrenergic receptor content was not changed. Conclusions: Topical epinephrine to limit blood loss during burn excision resulted in significant systemic absorption and increased plasma epinephrine levels. Acute sensitization of the lymphocytic β-adrenergic cascade was induced by the administration of epinephrine reflected by increased cAMP production after stimulation with isoproterenol and PGE 1. The lymphocytic β-adrenergic cascade exhibited homologous and heterologous desensitization 3 h after the use of epinephrine or thrombin, indicating that epinephrine administration was not a causative factor.

KW - Catecholamines

KW - Pediatrics

KW - Receptors

UR - http://www.scopus.com/inward/record.url?scp=0033867852&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033867852&partnerID=8YFLogxK

M3 - Article

VL - 93

SP - 351

EP - 358

JO - Anesthesiology

JF - Anesthesiology

SN - 0003-3022

IS - 2

ER -