...
首页> 外文期刊>Brazilian Journal of Medical and Biological Research >Intercostal and forearm muscle deoxygenation during respiratory fatigue in patients with heart failure: potential role of a respiratory muscle metaboreflex
【24h】

Intercostal and forearm muscle deoxygenation during respiratory fatigue in patients with heart failure: potential role of a respiratory muscle metaboreflex

机译:心力衰竭患者呼吸疲劳期间肋间和前臂肌肉脱氧:呼吸肌代谢反射的潜在作用

获取原文
           

摘要

The purpose of this study was to determine the effect of respiratory muscle fatigue on intercostal and forearm muscle perfusion and oxygenation in patients with heart failure. Five clinically stable heart failure patients with respiratory muscle weakness (age, 66±12 years; left ventricle ejection fraction, 34±3%) and nine matched healthy controls underwent a respiratory muscle fatigue protocol, breathing against a fixed resistance at 60% of their maximal inspiratory pressure for as long as they could sustain the predetermined inspiratory pressure. Intercostal and forearm muscle blood volume and oxygenation were continuously monitored by near-infrared spectroscopy with transducers placed on the seventh left intercostal space and the left forearm. Data were compared by two-way ANOVA and Bonferroni correction. Respiratory fatigue occurred at 5.1±1.3 min in heart failure patients and at 9.3±1.4 min in controls (P0.05), but perceived effort, changes in heart rate, and in systolic blood pressure were similar between groups (P0.05). Respiratory fatigue in heart failure reduced intercostal and forearm muscle blood volume (P0.05) along with decreased tissue oxygenation both in intercostal (heart failure, -2.6±1.6%; controls, +1.6±0.5%; P0.05) and in forearm muscles (heart failure, -4.5±0.5%; controls, +0.5±0.8%; P0.05). These results suggest that respiratory fatigue in patients with heart failure causes an oxygen demand/delivery mismatch in respiratory muscles, probably leading to a reflex reduction in peripheral limb muscle perfusion, featuring a respiratory metaboreflex.
机译:这项研究的目的是确定呼吸衰竭对心力衰竭患者肋间和前臂肌肉灌注和氧合的影响。 5例临床上稳定的心力衰竭患者出现呼吸肌无力(年龄66±12岁;左心室射血分数34±3%)和9名相匹配的健康对照组接受了呼吸肌疲劳方案,以60%的固定阻力呼吸最大吸气压力,只要它们可以维持预定的吸气压力即可。肋间和前臂肌肉的血容量和氧合通过近红外光谱法连续监测,换能器放置在左肋间第七处和左前臂。通过双向方差分析和Bonferroni校正比较数据。心力衰竭患者的呼吸疲劳发生在5.1±1.3 min,对照组的呼吸疲劳在9.3±1.4 min发生(P <0.05),但两组之间的感知努力,心率变化和收缩压相似(P> 0.05)。心力衰竭的呼吸疲劳减少肋间(心力衰竭,-2.6±1.6%;对照组,+ 1.6±0.5%; P <0.05)和前臂的肋间和前臂肌肉血容量(P <0.05)以及组织氧合减少。肌肉(心力衰竭,-4.5±0.5%;对照组,+ 0.5±0.8%; P <0.05)。这些结果表明,心力衰竭患者的呼吸疲劳会导致呼吸肌的供氧/供氧失配,可能导致周围肢体肌肉灌注反射降低,并伴有呼吸代谢反射。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号