Adams L, Lane R, Shea S A, Cockcroft A, Guz A
Clin Sci (Lond). 1985 Dec;69(6):663-72. doi: 10.1042/cs0690663.
This study investigates the mechanisms underlying the perception of breathlessness induced by hypoxia and hypercapnia in both naive normal subjects and patients with respiratory mechanical problems. In normal subjects separately receiving both oscillating hypercapnic and hypoxic ventilatory stimulation, equivalent peak stimulus intensities in end-tidal gas were associated with a 'damped' ventilatory response when the frequency of stimulation was increased. A concomitant fall in peak breathlessness levels on a visual analogue scale was recorded in each case. In normal subjects and patients, the voluntary copying of a ventilatory pattern recorded during oscillating hypercapnic stimulation was associated with a marked diminution or complete absence of breathlessness despite equivalent levels of peak ventilations achieved. Voluntary copying of hypercapnic stimulated ventilation was not associated with any demonstrable change in the distribution of muscle movements between the chest wall and abdomen. These results suggest that the intensity of breathlessness depends on the level of effective reflex stimulation of the respiratory-related neurones in the medulla. They cannot be explained solely in terms of perception of afferent neural information arising from either chemoreceptors or respiratory mechanoreceptors.
本研究调查了单纯正常受试者以及患有呼吸机械问题的患者中,由低氧和高碳酸血症诱发的呼吸急促感的潜在机制。在分别接受振荡性高碳酸血症和低氧通气刺激的正常受试者中,当刺激频率增加时,呼气末气体中等效的峰值刺激强度与“衰减”的通气反应相关。在每种情况下,视觉模拟量表上的峰值呼吸急促水平均伴随下降。在正常受试者和患者中,在振荡性高碳酸血症刺激期间记录的通气模式的自主模仿,与明显减轻或完全没有呼吸急促相关,尽管达到了等效的峰值通气水平。高碳酸血症刺激通气的自主模仿与胸壁和腹部之间肌肉运动分布的任何可证明的变化无关。这些结果表明,呼吸急促的强度取决于延髓中与呼吸相关的神经元的有效反射刺激水平。它们不能仅根据来自化学感受器或呼吸机械感受器的传入神经信息的感知来解释。