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轻度高血压患者运动后低血压的血流动力学和自主神经相关性

Hemodynamic and autonomic correlates of postexercise hypotension in patients with mild hypertension.

作者信息

Legramante Jacopo M, Galante Alberto, Massaro Michele, Attanasio Antonio, Raimondi Gianfranco, Pigozzi Fabio, Iellamo Ferdinando

机构信息

Dipartimento di Medicina Interna, Centro di Riabilitazione Cardiologica San Raffaele and Università di Roma Tor Vergata, 00173 Rome, Italy.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2002 Apr;282(4):R1037-43. doi: 10.1152/ajpregu.00603.2001.

DOI:10.1152/ajpregu.00603.2001
PMID:11893607
Abstract

We investigated the interplay of neural and hemodynamic mechanisms in postexercise hypotension (PEH) in hypertension. In 15 middle-aged patients with mild essential hypertension, we evaluated blood pressure (BP), cardiac output (CO), total peripheral resistance (TPR), forearm (FVR) and calf vascular resistance (CVR), and autonomic function [by spectral analysis of R-R interval and BP variabilities and spontaneous baroreflex sensitivity (BRS)] before and after maximal exercise. Systolic and diastolic BP, TPR, and CVR were significantly reduced from baseline 60-90 min after exercise. CO, FVR, and HR were unchanged. The low-frequency (LF) component of BP variability increased significantly after exercise, whereas the LF component of R-R interval variability was unchanged. The overall change in BRS was not significant after exercise vs. baseline, although a significant, albeit small, BRS increase occurred in response to hypotensive stimuli. These findings indicate that in hypertensive patients, PEH is mediated mainly by a peripheral vasodilation, which may involve metabolic factors linked to postexercise hyperemia in the active limbs. The vasodilator effect appears to override a concomitant, reflex sympathetic activation selectively directed to the vasculature, possibly aimed to counter excessive BP decreases. The cardiac component of arterial baroreflex is reset during PEH, although the baroreflex mechanisms controlling heart period appear to retain the potential for greater opposition to hypotensive stimuli.

摘要

我们研究了高血压患者运动后低血压(PEH)中神经和血流动力学机制的相互作用。在15名轻度原发性高血压中年患者中,我们评估了最大运动前后的血压(BP)、心输出量(CO)、总外周阻力(TPR)、前臂血管阻力(FVR)和小腿血管阻力(CVR),以及自主神经功能[通过R-R间期和血压变异性的频谱分析以及自发压力反射敏感性(BRS)]。运动后60 - 90分钟,收缩压和舒张压、TPR和CVR较基线显著降低。CO、FVR和心率未改变。运动后血压变异性的低频(LF)成分显著增加,而R-R间期变异性的LF成分未改变。与基线相比,运动后BRS的总体变化不显著,尽管对低血压刺激有显著(尽管较小)的BRS增加。这些发现表明,在高血压患者中,PEH主要由外周血管舒张介导,这可能涉及与运动后活跃肢体充血相关的代谢因素。血管舒张作用似乎超过了伴随的、选择性地针对血管系统的反射性交感神经激活,这可能旨在对抗过度的血压下降。在PEH期间,动脉压力反射的心脏成分被重置,尽管控制心动周期的压力反射机制似乎保留了对低血压刺激产生更大对抗的潜力。

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