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

Background: Burn patients have impaired myocardial function and decreased b eta-adrenergic responsiveness. Further beta-adrenergic dysfunction from sys temic absorption of topically administered epinephrine that Is given to lim it blood loss during bunt excision could affect perioperative management, T he authors evaluated the effect of topical epinephrine administration to pa tients during burn excision on the lymphocytic beta-adrenergic response. Methods: Fifty-five patients (age, 2-18 yr) with 20-90% body surface area b urns received a standardized anesthetic for a burn excision procedure. Lymp hocyte samples were taken at baseline and 1 and 3 h after the initial use o f epinephrine (n = 43) or thrombin (controls, n = 12), Plasma epinephrine l evels were measured by high-performance liquid chromatography, Lymphocyte b eta-adrenergic responsiveness was assessed by measuring production of cycli c adenosine monophosphate (cAMP) after stimulation with isoproterenol prost aglandin E-1 (PGE(1)) and forskolin, beta-adrenergic receptor binding assay s using iodopindolol and CGP12177 yielded beta-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 i n lymphocytes 1 h after epinephrine was greater in patients receiving epine phrine than In control patients on stimulation with isoproterenol (P < 0.05 ) and PGE, (P < 0.05). Three hours after epinephrine administration, produc tion 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 beta-adrene rgic receptor content was not changed. Conclusions: Topical epinephrine to limit blood loss during burn excision r esulted in significant systemic absorption and increased plasma epinephrine levels, Acute sensitization of the lymphocytic beta-adrenergic cascade was induced by the administration of epinephrine reflected by increased cAMP p roduction after stimulation with isoproterenol and PGE(1). The lymphocytic beta-adrenergic cascade exhibited homologous and heterologous desensitizati on 3 h after the use of epinephrine or thrombin, indicating that epinephrin e administration was not a causative factor.