Julius S
Schweiz Med Wochenschr. 1976 Dec 4;106(49):1698-705.
The systemic hemodynamic was investigated in 145 young male patients with borderline hypertension and 85 control subjects. Response of the cardiac output, stroke volume and the heart rate to sequential parasympathetic, beta-adrenergic and alpha-adrenergic blockade was used for assessment of the autonomic nervous tone. These investigations suggest that the apparently "innocent" minimal blood pressure elevation in borderline hypertension is associated with a number of physiologic abnormalities: The cardiac output, heart rate and stroke volume can be elevated. In all patients the peripheral resistance is abnormal. An abnormal distribution of plasma renin values is detectable. The plasma volume is decreased in a proportion of patients. A number of these abnormalities can be explained by a neurogenic mechanism. The elevation of the cardiac output is entirely neurogenic. In a substantial minority of patients, the elevation of peripheral resistance is attributable to increased sympathetic drive. Indirect evidence indicates that the plasma renin elevation in borderline hypertension may also be neurogenic. Hypothetically the decreased plasma volume may stem from sympathetic effects on postcapillary vessels, but at the present there is no experimental evidence of support this view. The change in autonomic function in borderline hypertension involves both the sympathetic and parasympathetic efferents. Increased sympathetic stimulation is coupled with decrease parasympathetic inhibition. This points toward abnormal integration of the autonomic control, presumably in the medulla oblongata. The mechanism of the autonomic abnormality is not fully elucidated. The role of baroreceptors requires further investigation. In some patients the altered autonomic integration appears to be related to psychosomatic mechanisms.
对145例临界高血压青年男性患者和85例对照者进行了全身血流动力学研究。通过心输出量、每搏输出量和心率对相继的副交感神经、β-肾上腺素能和α-肾上腺素能阻滞的反应来评估自主神经张力。这些研究表明,临界高血压中看似“无害”的轻度血压升高与一些生理异常有关:心输出量、心率和每搏输出量可能升高。所有患者的外周阻力均异常。可检测到血浆肾素值分布异常。部分患者的血浆容量减少。其中一些异常可用神经源性机制解释。心输出量的升高完全是神经源性的。在相当一部分少数患者中,外周阻力的升高归因于交感神经驱动增加。间接证据表明,临界高血压中血浆肾素升高也可能是神经源性的。据推测,血浆容量减少可能源于交感神经对毛细血管后血管的作用,但目前尚无支持这一观点的实验证据。临界高血压患者自主神经功能的改变涉及交感神经和副交感神经传出纤维。交感神经刺激增加与副交感神经抑制减少相关。这表明自主神经控制存在异常整合,推测发生在延髓。自主神经异常的机制尚未完全阐明。压力感受器的作用需要进一步研究。在一些患者中,自主神经整合改变似乎与身心机制有关。