Simon P M, Leevers A M, Murty J L, Skatrud J B, Dempsey J A
Medical Research Service, William S. Middleton Memorial Veterans Hospital, Madison 53705, USA.
J Appl Physiol (1985). 1995 Jul;79(1):312-23. doi: 10.1152/jappl.1995.79.1.312.
To evaluate the role of phrenic and sternocleidomastoid afferents as alternate sources of inhibitory feedback during mechanical ventilation, we studied five C2-C3 quadriplegics with sensory denervation of the rib cage and diaphragm, six C1-C2 quadriplegics with additional loss of sensory feedback from the neck muscles, and seven normal subjects. We compared the return of inspiratory muscle activity [the recruitment threshold (PCO2RT)] during mechanical ventilation between subject groups after stepwise increases in end-tidal PCO2 (PETCO2) either by increasing the inspired fraction of CO2 (FICO2), decreasing tidal volume (VT; 50 ml/min), or decreasing frequency (f; 1 breath/2 min). Normal subjects were mechanically hyperventilated via a nasal mask until inspiratory activity was undetectable. Efferent input to the sternocleidomastoid was intact at both levels of spinal cord injury, but phasic activity was not evident at the quadriplegics' baseline resting ventilation. The PCO2RT was defined as the level of PETCO2 at which phasic activity of the diaphragm in normal subjects and of the sternocleidomastoid in C1-C2 and C2-C3 quadriplegics recurred. The mean PCO2RT (in response to raising PETCO2 via increased FICO2 while maintaining a high VT and f) was not significantly different (P = 0.6) between normal subjects (43 +/- 3 Torr) and C2-C3 quadriplegics (38 +/- 5 Torr). Both subject groups demonstrated a frequency- and volume-related inhibition, as evidenced by a substantially lower PCO2RT when PETCO2 was raised by reducing either VT or f. In contrast to the C2-C3 quadriplegics, the C1-C2 quadriplegics responded with a similar PCO2RT among the three different mechanical ventilation trials, independent of whether PETCO2 was raised with high VT and f, with reduced VT, or with reduced f. We conclude that feedback from at least some part of the chest wall is required to produce a volume- and frequency-dependent inhibition of inspiratory muscle activity observed during mechanical ventilation.
为了评估在机械通气期间膈神经和胸锁乳突肌传入神经作为抑制性反馈替代来源的作用，我们研究了5名C2 - C3节段四肢瘫痪且胸廓和膈肌感觉神经去神经支配的患者、6名C1 - C2节段四肢瘫痪且颈部肌肉感觉反馈额外丧失的患者以及7名正常受试者。我们通过增加二氧化碳吸入分数（FICO2）、减少潮气量（VT；50 ml/分钟）或降低频率（f；1次呼吸/2分钟），逐步增加呼气末二氧化碳分压（PETCO2），比较了各受试者组在机械通气期间吸气肌活动的恢复情况[募集阈值（PCO2RT）]。正常受试者通过鼻罩进行机械性过度通气，直到吸气活动无法检测到。在两个脊髓损伤水平，胸锁乳突肌的传出输入均完整，但在四肢瘫痪患者的基线静息通气时，相位活动不明显。PCO2RT被定义为正常受试者膈肌以及C1 - C2和C2 - C3四肢瘫痪患者胸锁乳突肌相位活动再次出现时的PETCO2水平。正常受试者（43±3 Torr）和C2 - C3四肢瘫痪患者（38±5 Torr）之间的平均PCO2RT（通过增加FICO2同时维持高VT和f来提高PETCO2时）无显著差异（P = 0.6）。当通过降低VT或f来提高PETCO2时，两个受试者组均表现出与频率和容积相关的抑制，表现为PCO2RT显著降低。与C2 - C3四肢瘫痪患者不同，C1 - C2四肢瘫痪患者在三种不同的机械通气试验中具有相似的PCO2RT，无论PETCO2是通过高VT和f、降低VT还是降低f来提高。我们得出结论，在机械通气期间观察到的对吸气肌活动的容积和频率依赖性抑制，需要胸壁至少某些部分的反馈。
