Department of Critical Care Medicine, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Department of Emergency Medicine, Kurashiki Central Hospital, Kurashiki, Okayama, Japan.
J Appl Physiol (1985). 2022 Mar 1;132(3):622-631. doi: 10.1152/japplphysiol.00771.2020. Epub 2022 Feb 3.
Ventilatory response to sustained isocapnic hypoxia in adult humans and other mammals is characterized by a biphasic pattern, with attenuation of neuromotor output to the diaphragm. However, there is no a priori reason that hypoxia-mediated attenuation of respiratory drive would be a common event among other respiratory muscles. At present, little is known about the function of the chest wall muscles during sustained hypoxia. As an obligatory inspiratory muscle with potential to act as a surrogate for neural drive to the relatively inaccessible costal diaphragm, parasternal intercostal has gained interest clinically: its function during a sustained hypoxic insult, as may occur in respiratory failure, warrants investigation. Therefore, in 11 chronically instrumented awake canines, we simultaneously recorded muscle length and shortening and electromyogram (EMG) activity of the parasternal chest wall inspiratory muscle, along with breathing pattern, during moderate levels of sustained isocapnic hypoxia lasting 20-25 min (mean 80 ± 2% oximeter oxygen saturation). Phasic inspiratory shortening and EMG activity of the parasternal intercostal were observed throughout room air and hypoxic ventilation in all animals. Temporal changes in parasternal intercostal shortening tracked the biphasic changes in ventilation during sustained hypoxia. Mean shortening and EMG activity of parasternal intercostal muscle increased significantly with initial hypoxia ( < 0.01) and then markedly declined with constant hypoxia ( < 0.05). We conclude that attenuation of central neural respiratory drive extends to the primary chest wall inspiratory muscle, the parasternal intercostal, during sustained hypoxia, thus directly contributing to biphasic changes in ventilation. With the potential to act as a surrogate for the generally inaccessible costal diaphragm, parasternal intercostal has gained great interest clinically as a muscle to monitor neural drive and function in respiratory disease. This study demonstrates for the first time the impact of sustained hypoxia on neural activation and mechanical contraction of the parasternal intercostals. Parasternal intercostals reveal a biphasic action during the time-dependent hypoxic response, with a transient increase in shortening and EMG activity with acute hypoxia followed by a progressive decline when hypoxia is sustained.
成人和其他哺乳动物持续性等二氧化碳缺氧通气反应的特点是双相模式,膈神经运动输出减弱。然而,没有先验的理由表明缺氧介导的呼吸驱动减弱会在其他呼吸肌中普遍发生。目前,人们对持续性缺氧期间胸壁肌肉的功能知之甚少。作为一种强制性吸气肌,具有作为相对难以接近的肋膈神经驱动的替代物的潜力,胸骨旁肋间肌在临床上引起了兴趣:在呼吸衰竭等可能发生的持续性低氧刺激期间,其功能值得研究。因此,在 11 只慢性仪器化清醒犬中,我们同时记录了胸骨旁吸气肌的肌肉长度和缩短以及肌电图(EMG)活动,以及呼吸模式,在持续 20-25 分钟的中度持续性等二氧化碳缺氧期间(平均 80±2%血氧计氧饱和度)。在所有动物中,胸骨旁胸壁吸气肌在整个空气呼吸和低氧通气期间都观察到了相位性吸气缩短和 EMG 活动。胸骨旁肋间肌缩短的时间变化跟踪了持续性低氧期间通气的双相变化。随着初始缺氧(<0.01),胸骨旁肋间肌的平均缩短和 EMG 活动显著增加,然后随着持续缺氧(<0.05)明显下降。我们的结论是,持续性低氧时,中枢呼吸驱动的减弱延伸至主要的胸壁吸气肌,即胸骨旁肋间肌,从而直接导致通气的双相变化。胸骨旁肋间肌作为一种监测神经驱动和呼吸疾病中功能的肌肉,具有作为一般难以接近的肋膈神经的替代物的潜力,因此在临床上引起了极大的兴趣。这项研究首次证明了持续性缺氧对胸骨旁肋间肌的神经激活和机械收缩的影响。胸骨旁肋间肌在时间依赖性低氧反应中表现出双相作用,急性缺氧时缩短和 EMG 活动短暂增加,持续缺氧时逐渐下降。