Rouleau J L, Chatterjee K, Parmley W W, Kramer P, Swedberg K, Curran D, Namekawa M
Am Heart J. 1985 Feb;109(2):201-9. doi: 10.1016/0002-8703(85)90584-8.
To evaluate the effects of calcium entry blocking agents on cardiac sympathetic tone during angina pectoris, arterial and coronary sinus (CS) norepinephrine (NE) and epinephrine (E) concentrations and CS blood flow were determined at rest and during pacing-induced angina, both before and after verapamil in nine patients and after nifedipine in nine patients, all of whom had fixed obstructive coronary artery disease. Resting arterial NE and E concentrations and myocardial NE release and E uptake remained unchanged during angina before verapamil and nifedipine, suggesting unaltered systemic and cardiac sympathetic tone and myocardial E handling. Following verapamil and nifedipine, arterial NE and E concentrations remained unchanged. After verapamil, net myocardial NE release increased from 16,072 +/- 18,881 to 35,520 +/- 30,595 at preverapamil angina rate (p less than 0.01) and to 39,643 +/- 29,728 pg/min at postverapamil angina rate (p less than 0.01). NE release after nifedipine increased from -4207 +/- 8898 to 10,988 +/- 30,711 (p less than 0.05) at prenifedipine angina rate and to 19,942 +/- 26,644 pg/min (p less than 0.05) at postnifedipine angina rate. NE release was independent of changes in CS flow after verapamil or nifedipine. E uptake after verapamil and nifedipine remained unchanged. Although the precise mechanism is not known, myocardial alpha-adrenergic receptor blockage with verapamil and nifedipine remains a possible explanation for increased myocardial NE release.
为评估钙通道阻滞剂对心绞痛期间心脏交感神经张力的影响，测定了9例患者在静息状态下以及起搏诱发心绞痛期间，服用维拉帕米前后和9例患者服用硝苯地平后，动脉血和冠状窦（CS）中去甲肾上腺素（NE）和肾上腺素（E）的浓度以及CS血流量，所有患者均患有固定性阻塞性冠状动脉疾病。在服用维拉帕米和硝苯地平之前，心绞痛发作期间静息动脉血NE和E浓度、心肌NE释放及E摄取均未改变，提示全身和心脏交感神经张力以及心肌E处理未受影响。服用维拉帕米和硝苯地平后，动脉血NE和E浓度保持不变。服用维拉帕米后，在维拉帕米给药前心绞痛发作频率时，心肌NE净释放量从16,072±18,881增加至35,520±30,595（p<0.01），在维拉帕米给药后心绞痛发作频率时增加至39,643±29,728 pg/min（p<0.01）。服用硝苯地平后，在硝苯地平给药前心绞痛发作频率时NE释放量从-4207±8898增加至10,988±30,711（p<0.05），在硝苯地平给药后心绞痛发作频率时增加至19,942±26,644 pg/min（p<0.05）。服用维拉帕米或硝苯地平后，NE释放与CS血流量的变化无关。服用维拉帕米和硝苯地平后E摄取保持不变。尽管确切机制尚不清楚，但维拉帕米和硝苯地平导致的心肌α-肾上腺素能受体阻滞仍是心肌NE释放增加的一个可能解释。
