DEFECTIVE CARDIAC PARASYMPATHETIC CONTROL IN PATIENTS WITH HEART DISEASE
DEFECTIVE CARDIAC PARASYMPATHETIC CONTROL IN PATIENTS WITH HEART DISEASE
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DOI：
10.1056/nejm197110142851602
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发表时间：
1971-01-01
影响因子：
158.5
通讯作者：
BRAUNWALD, E
中科院分区：
文献类型：
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作者：
ECKBERG, DL;DRABINSKY, M;BRAUNWALD, E
为了确定心力衰竭时副交感神经系统的状态，在12名正常受试者和9名心脏病患者中用心得安进行肾上腺素能阻滞后，用阿托品进行副交感神经阻滞。阿托品使正常人的心率增加55 ± 9%，但心脏病患者的心率仅增加23 ± 8%（p <0.05）。在23名对照受试者和22名患者中，通过静脉注射苯肾上腺素产生动脉压的短暂升高，并将连续的R-R间期绘制为收缩压的函数。在正常人中，每单位动脉收缩压升高的心率减慢平均为16.0 ±1.8毫秒/毫米汞柱，而在患者中仅为3.70 ± 0.8毫秒/毫米汞柱（p <0.001）。压力感受器引起的正常人心率减慢被证明是由副交感神经系统介导的，因为它可以被阿托品消除。这些发现表明，心脏病患者的副交感神经心血管调节存在严重异常。
To define the state of the parasympathetic nervous system in heart failure, parasympathetic blockade with atropine was induced after adrenergic blockade with propranolol in 12 normal subjects and in nine patients with heart disease. Atropine elevated heart rate by 55 ± 9 per cent in normal subjects, but by only 23 ± 8 per cent in patients with heart disease (p less than 0.05). In 23 control subjects and 22 patients, transient elevations in arterial pressure were produced by intravenous injections of phenylephrine, and successive R-R intervals were plotted as a function of systolic pressure. The slowing of heart rate per unit rise in systolic arterial pressure averaged 16.0 ±1.8 msec per millimeter of mercury in normal subjects but only 3.70 ± 0.8 msec per millimeter of mercury in the patients (p less than 0.001). Baroreceptor-induced slowing of heart rate in normal subjects was shown to be mediated by the parasympathetic nervous system since it could be abolished with atropine. These findings point to a profound abnormality in parasympathetic cardiovascular regulation in heart disease.