Moriguchi A, Otsuka A, Kohara K, Mikami H, Katahira K, Tsunetoshi T, Higashimori K, Ohishi M, Yo Y, Ogihara T
Department of Geriatric Medicine, Osaka University Medical School, Japan.
Clin Auton Res. 1992 Aug;2(4):267-70. doi: 10.1007/BF01819547.
Spectral analysis of heart rate fluctuation was evaluated before and after administration of carteolol, a non-selective beta-adrenoceptor-blocker, to investigate the neural regulatory mechanisms underlying the haemodynamic changes induced by mental stress. Mental stress increased blood pressure and heart rate, with an increased low frequency band, and low frequency/high frequency ratio of the power spectral analysis which are indices of sympathetic activity. Carteolol did not change basal and pre-mental stress measurements of blood pressure, heart rate and spectral density. However, carteolol altered the response to mental stress with a decrease in spectral density of the low frequency band and low frequency/high frequency ratio, and an increase in the high frequency component. These results confirm that mental stress elevates blood pressure by activating the sympathetic nervous system, and suggest that blockade of the beta-adrenoceptor attenuates the pressor response by preventing the autonomic responses to mental stress.
在给予非选择性β-肾上腺素能受体阻滞剂卡替洛尔前后，对心率波动进行频谱分析，以研究精神应激诱导的血流动力学变化背后的神经调节机制。精神应激会使血压和心率升高，功率谱分析的低频带以及低频/高频比值增加，这些都是交感神经活动的指标。卡替洛尔并未改变血压、心率和频谱密度的基础值以及精神应激前的测量值。然而，卡替洛尔改变了对精神应激的反应，低频带的频谱密度和低频/高频比值降低，高频成分增加。这些结果证实精神应激通过激活交感神经系统升高血压，并表明β-肾上腺素能受体的阻断通过防止对精神应激的自主反应减弱升压反应。
