Role of sensory input from the lungs in control of muscle sympathetic nerve activity during and after apnea in humans.
Role of sensory input from the lungs in control of muscle sympathetic nerve activity during and after apnea in humans.
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来自肺部的感觉输入在人类呼吸暂停期间和之后控制肌肉交感神经活动中的作用。
DOI：
10.1152/japplphysiol.00241.2004
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Morgan,BarbaraJ
中科院分区：
文献类型：
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作者：
Khayat,RamiN;Przybylowski,Tadeusz;Meyer,KeithC;Skatrud,JamesB;Morgan,BarbaraJ
我们推测，如果肺充气反射对呼吸暂停诱导的交感神经激活有重要作用，则双侧肺移植受者(LTX)的这种激活将会减弱。我们测量了7名LTX和7名健康对照组(CON)在20-S呼气末屏气前、中和之后的肌交感神经活动、心率、平均动脉压、潮气量、呼气末二氧化碳分压和动脉血氧饱和度。我们的LTX失神经治疗的证据是：1)大大减轻了呼吸性窦性心律失常；2)隆突以下没有咳嗽反射。在呼吸暂停期间，LTX组和CON组MSNA的时间模式和峰值几乎相同(分别为基线的347±99和359±46%；P>；0.05)。相反，在恢复呼吸后的前5名S中，LTX组的MSNA含量高于对照组(分别为基线的101±4%和38±7%；P<；0.05)。在呼吸暂停引起的低氧血症或高碳酸血症、血流动力学或呼吸反应方面，两组之间没有差异。因此，在呼吸暂停时，停止正常情况下伴随的有节奏的交感神经抑制反馈对交感神经兴奋没有重要作用。相反，过度换气引起的肺伸展引起的迷走神经传入在呼吸暂停后恢复呼吸后产生的深刻、迅速的交感神经抑制中起着重要作用。
We reasoned that, if the lung inflation reflex contributes importantly to apnea-induced sympathetic activation, such activation would be attenuated in bilateral lung transplant recipients (LTX). We measured muscle sympathetic nerve activity (MSNA; intraneural electrodes), heart rate, mean arterial pressure, tidal volume, end-tidal Pco2, and arterial oxygen saturation in seven LTX and seven healthy control subjects (Con) before, during, and after 20-s end-expiratory breath holds. Our evidence for denervation in LTX was1) greatly attenuated respiratory sinus arrhythmia and2) absence of cough reflex below the level of the carina. During apnea, the temporal pattern and the peak increase in MSNA were virtually identical in LTX and Con (347 ± 99 and 359 ± 46% of baseline, respectively;P> 0.05). In contrast, the amount of MSNA present in the first 5 s after resumption of breathing was greater in LTX vs. Con (101 ± 4 vs. 38 ± 7% of baseline, respectively;P< 0.05). There were no between-group differences in apnea-induced hypoxemia or hypercapnia, hemodynamic, or ventilatory responses. Thus cessation of the rhythmic sympathoinhibitory feedback that normally accompanies eupneic breathing does not contribute importantly to sympathetic excitation during apnea. In contrast, vagal afferent input elicited by hyperventilation-induced lung stretch plays an important role in the profound, rapid sympathetic inhibition that occurs after resumption of breathing after apnea.