Craft N, Schwartz J B
Department of Medicine, University of California, San Francisco 94143, USA.
Am J Physiol. 1995 Apr;268(4 Pt 2):H1441-52. doi: 10.1152/ajpheart.1995.268.4.H1441.
Heart rate, heart rate variability, and atrioventricular (AV) conduction were studied in 20 young (30 +/- 5 yr) and 19 older (69 +/- 7 yr) healthy men and women before and after single and double autonomic blockade (randomized order: atropine, 0.04 mg/kg i.v.; propranolol, 0.2 mg/kg i.v.). Basal R-R intervals did not differ, but older age increased P-R intervals (177 +/- 24 vs. 149 +/- 17 ms, P < 0.001) and decreased SD of R-R (43 +/- 17 vs. 70 +/- 18 ms, P = 0.001) and heart rate spectral content (area under the power vs. frequency curve from 0.04 to 0.32 Hz: 3.01 +/- 2.1 vs. 7.82 +/- 4.8 beats/min2, P < 0.009), as well as postural responses (R-R decreases of 107 +/- 80 vs. 250 +/- 72 ms, P < 0.002). Atropine decreased R-R intervals, SD of R-R, and high-frequency (0.24-0.32 Hz) spectral content less in elderly subjects compared with younger subjects. Propranolol increased R-R and P-R intervals equally in old and young and abolished low-frequency (0.04-0.12 Hz) increases with standing (P < 0.0008). After double blockade, R-R, P-R, and paced AV intervals were longer in old subjects. Mean values were as follows: R-R intervals, 859 +/- 176 vs. 677 +/- 106 ms, P < 0.001; P-R intervals, 179 +/- 23 vs. 149 +/- 17 ms, P = 0.0002; paced P-R intervals (500 ms), 251 +/- 39 vs. 215 +/- 47 ms; and AV block cycle length, 413 +/- 51 vs. 385 +/- 69 ms (multivariate analysis of variance, P < 0.03). After double autonomic blockade, heart rate variability was nearly eliminated in young and old (reduced > 98%, P < 0.0001). We conclude that age differences in heart rate variability can be explained by autonomic influences, but heart rate and AV conduction differences exist independently of beta-adrenergic and/or parasympathetic influences.
在20名年轻(30±5岁)和19名年长(69±7岁)的健康男性和女性中,研究了单重和双重自主神经阻滞(随机顺序:静脉注射0.04mg/kg阿托品;静脉注射0.2mg/kg普萘洛尔)前后的心率、心率变异性和房室(AV)传导。基础R-R间期无差异,但年长使P-R间期延长(177±24对149±17ms,P<0.001),R-R标准差降低(43±17对70±18ms,P=0.001),心率频谱含量降低(功率与频率曲线下0.04至0.32Hz的面积:3.01±2.1对7.82±4.8次/分钟²,P<0.009),以及体位反应降低(R-R降低107±80对250±72ms,P<0.002)。与年轻受试者相比,阿托品使年长受试者的R-R间期、R-R标准差和高频(0.24 - 0.32Hz)频谱含量降低幅度更小。普萘洛尔使年轻和年长受试者的R-R和P-R间期同等增加,并消除了站立时低频(0.04 - 0.12Hz)的增加(P<0.0008)。双重阻滞后,年长受试者的R-R、P-R和起搏房室间期更长。平均值如下:R-R间期,859±176对677±106ms,P<0.001;P-R间期,179±23对149±17ms,P = 0.0002;起搏P-R间期(500ms),251±39对215±47ms;以及房室传导周期长度,413±51对385±69ms(多变量方差分析,P<0.03)。双重自主神经阻滞后,年轻和年长受试者的心率变异性几乎完全消除(降低>98%,P<0.0001)。我们得出结论,心率变异性的年龄差异可由自主神经影响来解释,但心率和房室传导差异独立于β-肾上腺素能和/或副交感神经影响而存在。