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在动态运动过程中,动脉压力反射会改变肌肉代谢反射的强度和机制。

Arterial baroreflex alters strength and mechanisms of muscle metaboreflex during dynamic exercise.

作者信息

Kim Jong-Kyung, Sala-Mercado Javier A, Rodriguez Jaime, Scislo Tadeusz J, O'Leary Donal S

机构信息

Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.

出版信息

Am J Physiol Heart Circ Physiol. 2005 Mar;288(3):H1374-80. doi: 10.1152/ajpheart.01040.2004. Epub 2004 Nov 11.

Abstract

Previous studies showed that the arterial baroreflex opposes the pressor response mediated by muscle metaboreflex activation during mild dynamic exercise. However, no studies have investigated the mechanisms contributing to metaboreflex-mediated pressor responses during dynamic exercise after arterial baroreceptor denervation. Therefore, we investigated the contribution of cardiac output (CO) and peripheral vasoconstriction in mediating the pressor response to graded reductions in hindlimb perfusion in conscious, chronically instrumented dogs before and after sinoaortic denervation (SAD) during mild and moderate exercise. In control experiments, the metaboreflex pressor responses were mediated via increases in CO. After SAD, the metaboreflex pressor responses were significantly greater and significantly smaller increases in CO occurred. During control experiments, nonischemic vascular conductance (NIVC) did not change with muscle metaboreflex activation, whereas after SAD NIVC significantly decreased with metaboreflex activation; thus SAD shifted the mechanisms of the muscle metaboreflex from mainly increases in CO to combined cardiac and peripheral vasoconstrictor responses. We conclude that the major mechanism by which the arterial baroreflex buffers the muscle metaboreflex is inhibition of metaboreflex-mediated peripheral vasoconstriction.

摘要

先前的研究表明,在轻度动态运动期间,动脉压力反射会对抗由肌肉代谢反射激活介导的升压反应。然而,尚无研究探讨动脉压力感受器去神经支配后动态运动期间代谢反射介导的升压反应的机制。因此,我们研究了在轻度和中度运动期间,在慢性植入仪器的清醒犬进行主动脉弓和颈动脉窦去神经支配(SAD)前后,心输出量(CO)和外周血管收缩在介导后肢灌注分级降低的升压反应中的作用。在对照实验中,代谢反射升压反应是通过CO的增加介导的。SAD后,代谢反射升压反应明显更大,而CO的增加明显更小。在对照实验期间,非缺血性血管传导(NIVC)不会随着肌肉代谢反射激活而改变,而在SAD后,NIVC会随着代谢反射激活而显著降低;因此,SAD将肌肉代谢反射的机制从主要是CO增加转变为心脏和外周血管收缩反应的联合作用。我们得出结论,动脉压力反射缓冲肌肉代谢反射的主要机制是抑制代谢反射介导的外周血管收缩。

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