McQuitty C K, Berman J, Cortiella J, Herndon D, Mathru M
Departments of Anesthesiology, Internal Medicine, and Surgery, The University of Texas Medical Branch and Shriners Burns Institute, Galveston, 77555-0591, USA.
Anesthesiology. 2000 Aug;93(2):351-8. doi: 10.1097/00000542-200008000-00012.
Burn patients have impaired myocardial function and decreased beta-adrenergic responsiveness. Further beta-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 beta-adrenergic response.
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 beta-adrenergic responsiveness was assessed by measuring production of cyclic adenosine monophosphate (cAMP) after stimulation with isoproterenol, prostaglandin E1 (PGE1), and forskolin. beta-adrenergic receptor binding assays using iodopindolol and CGP12177 yielded beta-adrenergic receptor density.
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 PGE1 (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), PGE1(P < 0.05), and forskolin (P < 0.05). Lymphocytic beta-adrenergic receptor content was not changed.
Topical epinephrine to limit blood loss during burn excision resulted 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 production after stimulation with isoproterenol and PGE1. The lymphocytic beta-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.
烧伤患者存在心肌功能受损和β-肾上腺素能反应性降低的情况。在烧伤清创术中用于限制失血的局部应用肾上腺素经全身吸收导致的进一步β-肾上腺素能功能障碍可能会影响围手术期管理。作者评估了烧伤清创术中给患者局部应用肾上腺素对淋巴细胞β-肾上腺素能反应的影响。
55例（年龄2至18岁）烧伤面积为20%至90%体表面积的患者接受了标准化麻醉以进行烧伤清创手术。在基线时以及首次使用肾上腺素（n = 43）或凝血酶（对照组，n = 12）后1小时和3小时采集淋巴细胞样本。通过高效液相色谱法测量血浆肾上腺素水平。通过测量用异丙肾上腺素、前列腺素E1（PGE1）和福斯高林刺激后环磷酸腺苷（cAMP）的生成来评估淋巴细胞β-肾上腺素能反应性。使用碘吲哚洛尔和CGP12177进行β-肾上腺素能受体结合试验得出β-肾上腺素能受体密度。
使用肾上腺素后1小时（P < 0.01）和3小时（P < 0.01）肾上腺素水平升高，但对照组患者未升高。在用异丙肾上腺素（P < 0.05）和PGE1（P < 0.05）刺激后，接受肾上腺素的患者在使用肾上腺素后1小时淋巴细胞中cAMP的生成量高于对照组患者。在使用肾上腺素3小时后，与基线相比，对照组患者以及接受肾上腺素的患者在用异丙肾上腺素（P < 0.05）、PGE1（P < 0.05）和福斯高林（P < 0.05）刺激后cAMP的生成量均减少。淋巴细胞β-肾上腺素能受体含量未改变。
在烧伤清创术中局部应用肾上腺素以限制失血导致了显著的全身吸收并提高了血浆肾上腺素水平。肾上腺素的应用诱导了淋巴细胞β-肾上腺素能级联反应的急性致敏，这表现为用异丙肾上腺素和PGE1刺激后cAMP生成增加。在使用肾上腺素或凝血酶3小时后，淋巴细胞β-肾上腺素能级联反应表现出同源和异源脱敏，这表明肾上腺素的应用不是一个致病因素。
