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高血压时减弱的肌肉代谢反射引起的心脏功能增加。

Attenuated muscle metaboreflex-induced increases in cardiac function in hypertension.

机构信息

Department of Physiology and The Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan.

出版信息

Am J Physiol Heart Circ Physiol. 2013 Nov 15;305(10):H1548-54. doi: 10.1152/ajpheart.00478.2013. Epub 2013 Sep 6.


DOI:10.1152/ajpheart.00478.2013
PMID:24014673
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3840258/
Abstract

Sympathoactivation may be excessive during exercise in subjects with hypertension, leading to increased susceptibility to adverse cardiovascular events, including arrhythmias, infarction, stroke, and sudden cardiac death. The muscle metaboreflex is a powerful cardiovascular reflex capable of eliciting marked increases in sympathetic activity during exercise. We used conscious, chronically instrumented dogs trained to run on a motor-driven treadmill to investigate the effects of hypertension on the mechanisms of the muscle metaboreflex. Experiments were performed before and 30.9 ± 4.2 days after induction of hypertension, which was induced via partial, unilateral renal artery occlusion. After induction of hypertension, resting mean arterial pressure was significantly elevated from 98.2 ± 2.6 to 141.9 ± 7.4 mmHg. The hypertension was caused by elevated total peripheral resistance. Although cardiac output was not significantly different at rest or during exercise after induction of hypertension, the rise in cardiac output with muscle metaboreflex activation was significantly reduced in hypertension. Metaboreflex-induced increases in left ventricular function were also depressed. These attenuated cardiac responses caused a smaller metaboreflex-induced rise in mean arterial pressure. We conclude that the ability of the muscle metaboreflex to elicit increases in cardiac function is impaired in hypertension, which may contribute to exercise intolerance.

摘要

在高血压患者运动时,交感神经可能会过度激活,导致易发生不良心血管事件,包括心律失常、梗死、中风和心源性猝死。肌肉代谢反射是一种强大的心血管反射,能够在运动过程中引起交感神经活动的显著增加。我们使用经过训练的清醒、慢性仪器化的狗,在电动跑步机上跑步,以研究高血压对肌肉代谢反射机制的影响。实验在诱导高血压前和诱导高血压后 30.9 ± 4.2 天进行,高血压是通过部分单侧肾动脉阻塞诱导的。诱导高血压后,静息平均动脉压从 98.2 ± 2.6mmHg 显著升高至 141.9 ± 7.4mmHg。高血压是由总外周阻力升高引起的。尽管诱导高血压后静息或运动时的心输出量没有显著差异,但肌肉代谢反射激活时心输出量的增加在高血压中显著减少。代谢反射引起的左心室功能增加也受到抑制。这些减弱的心脏反应导致代谢反射引起的平均动脉压升高较小。我们的结论是,肌肉代谢反射引起的心脏功能增加的能力在高血压中受损,这可能导致运动不耐受。

相似文献

[1]
Attenuated muscle metaboreflex-induced increases in cardiac function in hypertension.

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[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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[4]
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[5]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Augmentation of the exercise pressor reflex in prehypertension: roles of the muscle metaboreflex and mechanoreflex.

Appl Physiol Nutr Metab. 2013-2-14

[2]
Role of cardiac output versus peripheral vasoconstriction in mediating muscle metaboreflex pressor responses: dynamic exercise versus postexercise muscle ischemia.

Am J Physiol Regul Integr Comp Physiol. 2013-2-20

[3]
Muscle metaboreflex-induced coronary vasoconstriction limits ventricular contractility during dynamic exercise in heart failure.

Am J Physiol Heart Circ Physiol. 2013-1-25

[4]
Antagonism of the TRPv1 receptor partially corrects muscle metaboreflex overactivity in spontaneously hypertensive rats.

J Physiol. 2011-10-24

[5]
Role of heart rate and stroke volume during muscle metaboreflex-induced cardiac output increase: differences between activation during and after exercise.

J Physiol Sci. 2011-7-28

[6]
Skeletal muscle reflex-mediated changes in sympathetic nerve activity are abnormal in spontaneously hypertensive rats.

Am J Physiol Heart Circ Physiol. 2011-1-7

[7]
Exaggerated sympathetic and pressor responses to handgrip exercise in older hypertensive humans: role of the muscle metaboreflex.

Am J Physiol Heart Circ Physiol. 2010-8-27

[8]
Group III and IV muscle afferents contribute to ventilatory and cardiovascular response to rhythmic exercise in humans.

J Appl Physiol (1985). 2010-7-15

[9]
Neuronal nitric oxide synthase within paraventricular nucleus: blood pressure and baroreflex in two-kidney, one-clip hypertensive rats.

Exp Physiol. 2010-5-21

[10]
Muscle metaboreflex-induced coronary vasoconstriction functionally limits increases in ventricular contractility.

J Appl Physiol (1985). 2010-8

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