Morady F, Nelson S D, Kou W H, Pratley R, Schmaltz S, De Buitleir M, Halter J B
Division of Cardiology, University of Michigan Medical Center, Ann Arbor.
J Am Coll Cardiol. 1988 Jun;11(6):1235-44. doi: 10.1016/0735-1097(88)90287-2.
The electrophysiologic effects of circulating epinephrine in humans were examined in four study groups of 10 subjects each. In 10 subjects without structural heart disease (Group 1) and in 10 patients with coronary disease or dilated cardiomyopathy (Group 2) epinephrine infusion at 25 and 50 ng/kg body weight per min for 14 min resulted in an elevation of the plasma epinephrine concentration in the physiologic range. In both groups it produced a dose-dependent decrease in the effective refractory period of the atrium, atrioventricular (AV) node and ventricle and improvement in AV node conduction. Epinephrine facilitated the induction of sustained ventricular tachycardia in 3 of the 20 subjects. In Group 3, a beta-adrenergic blocking dose of propranolol was added to the infusion of 50 ng/kg per min of epinephrine. Propranolol not only reversed the effects of epinephrine, but also lengthened these variables compared with baseline values. In Group 4, propranolol was administered first, followed by 50 ng/kg per min of epinephrine. Propranolol alone slowed AV node conduction and mildly prolonged the refractory periods. In the presence of beta-blockade, epinephrine had no effect on AV node properties but resulted in a lengthening of the atrial and ventricular effective refractory periods. In conclusion, epinephrine in physiologic doses shortens the effective refractory period of the atrium, AV node and ventricle, improves AV node conduction and may facilitate the induction of sustained ventricular tachycardia. The overall electrophysiologic effects of epinephrine result from stimulation of beta-receptors. Stimulation of alpha-receptors by epinephrine has no effect on the AV node but prolongs the effective refractory period of the atrium and ventricle, partially offsetting the shortening of refractory periods mediated by beta-receptor stimulation.
对四组研究对象进行了研究，每组10名受试者，以检验循环肾上腺素对人体的电生理效应。在10名无结构性心脏病的受试者（第1组）和10名患有冠心病或扩张型心肌病的患者（第2组）中，以每分钟25和50 ng/kg体重的剂量静脉输注肾上腺素14分钟，可使血浆肾上腺素浓度升高至生理范围。在两组中，它均使心房、房室（AV）结和心室的有效不应期呈剂量依赖性缩短，并改善了房室结传导。肾上腺素促使20名受试者中的3人诱发持续性室性心动过速。在第3组中，在每分钟50 ng/kg肾上腺素输注中加入β-肾上腺素能阻滞剂普萘洛尔。普萘洛尔不仅逆转了肾上腺素的作用，而且与基线值相比还延长了这些变量。在第4组中，先给予普萘洛尔，然后以每分钟50 ng/kg的剂量静脉输注肾上腺素。单独使用普萘洛尔可减慢房室结传导，并轻度延长不应期。在存在β-阻滞剂的情况下，肾上腺素对房室结特性无影响，但可导致心房和心室有效不应期延长。总之，生理剂量的肾上腺素可缩短心房、房室结和心室的有效不应期，改善房室结传导，并可能促使诱发持续性室性心动过速。肾上腺素的总体电生理效应是由β受体刺激引起的。肾上腺素对α受体的刺激对房室结无影响，但可延长心房和心室的有效不应期，部分抵消由β受体刺激介导的不应期缩短。
