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首页> 外文期刊>American Journal of Physiology >Exercise metaboreflex activation and endothelial function impairment in atrial fibrillation.
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Exercise metaboreflex activation and endothelial function impairment in atrial fibrillation.

机译：心房颤动时运动代谢反射激活和内皮功能受损。

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摘要

Exercising muscle hypoperfusion stimulates afferents (metaboreceptors) involved in the regulation of ventilation. Atrial fibrillation (AF), particularly when combined with diseases causing endothelial (ED) impairment, such as hypertension (HP) and diabetes mellitus (DM), depresses the ED activity and enhances exercise hyperventilation. The relationship between these two functions and the underlying mechanisms have not been explored previously. In lone AF or AF associated with HP or DM (12 subjects in each cohort), we investigated the brachial artery flow-mediated dilatation (ED function) and ventilation during the recovery phase of handgrip (metaboreflex) exercise for subjects receiving placebo or oral vitamin C (double-blind crossover), both before and after cardioversion (CV) to sinus rhythm. Baseline ED impairment was increasingly more severe and the ergoreflex activity more pronounced in AF + HP and AF + DM compared with lone AF. Vitamin C and CV significantly improved both flow-mediated dilatationand metaboreflex activity in lone AF and AF + HP, and vitamin C did not produce any additive effect when administered after CV. In AF + DM, neither vitamin C nor CV was effective. This study provides the following information: AF generates oxidative injury, which is less when the arrhythmia is lone AF and greater when the arrhythmia is associated with HP. In DM, the oxidative injury generated by AF is refractory to a rather weak antioxidant, like vitamin C, or the baseline damage is such as to prevent any additive influence of AF. In AF, a cause-effect link exists between ED dysfunction and metaboreflex activity. Ventilatory advantages of CV seem to be inversely related with the extension of the underlying ED oxidative impairment.
机译：锻炼肌肉灌注不足会刺激参与通气调节的传入（代谢受体）。心房颤动（AF），尤其是与导致内皮（ED）损伤的疾病（例如高血压（HP）和糖尿病（DM））结合使用时，会降低ED活性并增强运动过度换气。这两个功能与基本机制之间的关系以前未曾探讨过。在单独的AF或与HP或DM相关的AF（每组12名受试者）中，我们研究了接受安慰剂或口服维生素的受试者在手法运动（代谢反射）恢复阶段的肱动脉血流介导的扩张（ED功能）和通气C（双盲交叉），在心脏复律（CV）之前和之后到窦性心律。与单独的AF相比，AF + HP和AF + DM的基线ED损伤越来越严重，而全反射运动更为明显。维生素C和CV可以显着改善孤独房颤和AF + HP的血流介导的扩张和代谢反射活性，而CV给药后维生素C不会产生任何累加作用。在AF + DM中，维生素C和CV均无效。该研究提供以下信息：AF产生氧化损伤，当心律不齐为单独的AF时较少，而与HP相关的心律不齐时则更大。在DM中，由AF产生的氧化性损伤对于相当弱的抗氧化剂（如维生素C）是难治的，或者基线损伤是为了防止AF产生任何附加影响。在AF中，ED功能障碍和代谢反射活性之间存在因果关系。 CV的通气优势似乎与潜在的ED氧化损伤的扩展成反比。

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