Pokorski M, Morikawa T, Takaishi S, Masuda A, Ahn B, Honda Y
Department of Physiology, School of Medicine, Chiba University, Japan.
Eur Respir J. 1990 Sep;3(8):891-900.
We tested the hypothesis that interruption of motor traffic running down the spinal cord to respiratory muscle motoneurons suppresses the ventilatory response to increased chemical drive. We compared the hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses, based on the rebreathing technique, before and during inspiratory flow-resistive loading in 17 quadriplegic patients with low cervical spinal cord transection and in 17 normal subjects. The ventilatory response was evaluated from minute ventilation (VE) and mouth occlusion pressure (P0.2) slopes on arterial oxygen saturation (SaO2) or on end-tidal PCO2 (PACO2), and from absolute VE values at SaO2 80% or at PACO2 55 mmHg. We found no difference in the unloaded HVR or HCVR between the quadriplegic and normal subjects. In the loaded HVR, the delta VE/delta SaO2 slope tended to decrease similarly in both groups of subjects. The delta P0.2/delta SaO2 slope was shifted upwards in normal subjects, yielding a significantly higher P0.2 at a given SaO2. In contrast, this rise in the P0.2 level during loaded HVR was absent in quadriplegics. Loaded HCVR yielded qualitatively similar results in both groups of subjects; delta VE/delta PACO2 decreased and delta P0.2/delta PACO2 increased significantly. The results show that the ventilatory chemosensory responses were unsuppressed in quadriplegics, although they displayed a disturbance in load-compensation, as reflected by occlusion pressure, in hypoxia. We conclude that the descending drive to respiratory muscle motoneurons is not germane to the operation of the chemosensory reflexes.
中断沿脊髓下行至呼吸肌运动神经元的运动信号会抑制对化学驱动增加的通气反应。我们比较了17例颈髓低位横断的四肢瘫痪患者和17名正常受试者在吸气时进行气流阻力负荷前后,基于重复呼吸技术的低氧通气反应(HVR)和高碳酸通气反应(HCVR)。根据动脉血氧饱和度(SaO2)或呼气末二氧化碳分压(PACO2)时的分钟通气量(VE)和口腔阻断压(P0.2)斜率,以及在SaO2 80%或PACO2 55 mmHg时的绝对VE值来评估通气反应。我们发现四肢瘫痪患者和正常受试者在无负荷的HVR或HCVR方面没有差异。在有负荷的HVR中,两组受试者的ΔVE/ΔSaO2斜率均有类似下降趋势。正常受试者的ΔP0.2/ΔSaO2斜率上移,在给定的SaO2水平下产生显著更高的P0.2。相比之下,四肢瘫痪患者在有负荷的HVR期间P0.2水平没有升高。两组受试者在有负荷的HCVR方面产生了定性相似的结果;ΔVE/ΔPACO2下降,ΔP0.2/ΔPACO2显著增加。结果表明,四肢瘫痪患者的通气化学感受反应并未受到抑制,尽管在低氧时,如通过阻断压所反映的,他们在负荷补偿方面存在障碍。我们得出结论,下行至呼吸肌运动神经元的驱动与化学感受反射的运作无关。