Raux Mathieu, Straus Christian, Redolfi Stefania, Morelot-Panzini Capucine, Couturier Antoine, Hug François, Similowski Thomas
Université Pierre et Marie Curie-Paris6, UPRES EA 2397, Paris, France.
J Physiol. 2007 Jan 15;578(Pt 2):569-78. doi: 10.1113/jphysiol.2006.120246. Epub 2006 Nov 16.
Faced with mechanical inspiratory loading, awake animals and anaesthetized humans develop alveolar hypoventilation, whereas awake humans do defend ventilation. This points to a suprapontine compensatory mechanism instead of or in addition to the 'traditional' brainstem respiratory regulation. This study assesses the role of the cortical pre-motor representation of inspiratory muscles in this behaviour. Ten healthy subjects (age 19-34 years, three men) were studied during quiet breathing, CO2-stimulated breathing, inspiratory resistive loading, inspiratory threshold loading, and during self-paced voluntary sniffs. Pre-triggered ensemble averaging of Cz EEG epochs starting 2.5 s before the onset of inspiration was used to look for pre-motor activity. Pre-motor potentials were present during voluntary sniffs in all subjects (average latency (+/-s.d.): 1325 +/- 521 ms), but also during inspiratory threshold loading (1427 +/- 537 ms) and during inspiratory resistive loading (1109 +/- 465 ms). Pre-motor potentials were systematically followed by motor potentials during inspiratory loading. Pre-motor potentials were lacking during quiet breathing (except in one case) and during CO2-stimulated breathing (except in two cases). The same pattern was observed during repeated experiments at an interval of several weeks in a subset of three subjects. The behavioural component of inspiratory loading compensation in awake humans could thus depend on higher cortical motor areas. Demonstrating a similar role of the cerebral cortex in the compensation of disease-related inspiratory loads (e.g. asthma attacks) would have important pathophysiological implications: it could for example contribute to explain why sleep is both altered and deleterious in such situations.
面对机械性吸气负荷时,清醒的动物和麻醉的人类会出现肺泡通气不足,而清醒的人类确实会维持通气。这表明存在一种脑桥上的代偿机制,而非“传统的”脑干呼吸调节机制,或者是除脑干呼吸调节机制之外还存在这种脑桥上的代偿机制。本研究评估了吸气肌的皮质运动前表征在这种行为中的作用。对10名健康受试者(年龄19 - 34岁,3名男性)在安静呼吸、二氧化碳刺激呼吸、吸气阻力负荷、吸气阈值负荷以及自主控制的随意吸气过程中进行了研究。通过对吸气开始前2.5秒开始的Cz脑电图段进行预触发总体平均,来寻找运动前活动。在所有受试者的随意吸气过程中(平均潜伏期(±标准差):1325 ± 521毫秒)均存在运动前电位,在吸气阈值负荷时(1427 ± 537毫秒)以及吸气阻力负荷时(1109 ± 465毫秒)也存在运动前电位。在吸气负荷期间,运动前电位之后会系统性地出现运动电位。在安静呼吸时(除1例)以及二氧化碳刺激呼吸时(除2例)不存在运动前电位。在3名受试者的一个亚组中,间隔数周进行的重复实验中观察到了相同的模式。因此,清醒人类吸气负荷代偿的行为成分可能依赖于更高层次的皮质运动区域。证明大脑皮质在与疾病相关的吸气负荷(如哮喘发作)的代偿中具有类似作用将具有重要的病理生理学意义:例如,这可能有助于解释为什么在这种情况下睡眠会发生改变且有害。