Schwinn D A, McIntyre R W, Hawkins E D, Kates R A, Reves J G
Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina 27710.
Anesthesiology. 1988 Aug;69(2):206-17. doi: 10.1097/00000542-198808000-00009.
Elevated catecholamines and beta-adrenergic receptor hyporesponsiveness (or desensitization) have been demonstrated in failing human myocardium, but the role of the alpha-adrenergic receptor remains unclear. The authors tested the hypothesis that alpha 1-adrenergic responsiveness decreases in patients with impaired ventricular function undergoing coronary artery revascularization. Impaired ventricular function was defined prospectively by left ventricular ejection fraction less than or equal to 40% (group I, n = 12), and normal ventricular function by ejection fraction greater than 40% (group II, n = 22). Phenylephrine (Phe) pressor dose-response curves were established prior to anesthesia, during fentanyl anesthesia, and during fentanyl anesthesia plus hypothermic cardiopulmonary bypass at the time of aortic cross-clamp (anes + CPB/AXC). Polynomial regression of the Phe dose response curve estimated the Phe dose required to increase mean arterial blood pressure 20%, designated PD20. Although pre-anesthesia PD20 and anes + CPB/AXC PD20 values were not affected by ejection fraction, significant differences in PD20 (P less than 0.05) between groups occurred during fentanyl anesthesia (group I = 2.28 +/- 1.60 micrograms.kg-1, group II 1.57 +/- 0.98 micrograms.kg-1; mean +/- SD). Anes + CPB/AXC was associated with a significant reduction in PD20 in both groups compared with pre-anesthesia (P less than 0.01). Our results suggest impairment of alpha 1-adrenergic responsiveness occurs during fentanyl anesthesia in patients with ejection fractions less than or equal to 40% (evidenced by greater PD20 values). Although this impairment may be due to altered Phe pharmacokinetics, these results also support the possible existance of alpha 1-adrenergic receptor desensitization in this group. Reduction in PD20 during anes + CPB/AXC in all patients points to more powerful effects than fentanyl anesthesia alone; such influencing effects may include hemodilution, hypothermia, elevated plasma catecholamines, exclusion of the pulmonary circulation, or altered Phe pharmacokinetics.
在衰竭的人体心肌中已证实儿茶酚胺水平升高以及β-肾上腺素能受体反应性降低（或脱敏），但α-肾上腺素能受体的作用仍不清楚。作者检验了以下假设：接受冠状动脉血运重建的心室功能受损患者，其α1-肾上腺素能反应性降低。前瞻性地将心室功能受损定义为左心室射血分数小于或等于40%（I组，n = 12），将心室功能正常定义为射血分数大于40%（II组，n = 22）。在麻醉前、芬太尼麻醉期间以及主动脉阻断时的芬太尼麻醉加低温体外循环期间（麻醉+体外循环/主动脉阻断）建立去氧肾上腺素（Phe）升压剂量反应曲线。Phe剂量反应曲线的多项式回归估计使平均动脉血压升高20%所需的Phe剂量，称为PD20。尽管麻醉前的PD20值和麻醉+体外循环/主动脉阻断时的PD20值不受射血分数影响，但在芬太尼麻醉期间两组之间的PD20存在显著差异（P < 0.05）（I组= 2.28±1.60微克·千克-1，II组1.57±0.98微克·千克-1；均值±标准差）。与麻醉前相比，两组在麻醉+体外循环/主动脉阻断时的PD20均显著降低（P < 0.01）。我们的结果表明，射血分数小于或等于40%的患者在芬太尼麻醉期间会出现α1-肾上腺素能反应性受损（以更高的PD20值为证）。虽然这种损害可能是由于Phe药代动力学改变，但这些结果也支持该组中可能存在α1-肾上腺素能受体脱敏。所有患者在麻醉+体外循环/主动脉阻断期间PD20降低表明其作用比单独的芬太尼麻醉更强；这种影响作用可能包括血液稀释、低温、血浆儿茶酚胺升高、肺循环排除或Phe药代动力学改变。
