Haouzi Philippe, Chenuel Bruno, Whipp Brian J
Laboratoire de Physiologie, Faculté de Médecine de Nancy, EA 3450, Université H. Poincaré, France.
Respir Physiol Neurobiol. 2007 Nov 15;159(2):211-8. doi: 10.1016/j.resp.2007.07.008. Epub 2007 Jul 31.
This study addresses the following question: does the ventilatory control system adjust total ventilation in accord with the regulatory demands of the physiological dead space ventilation (VD) when the breathing frequency changes, and if so, how? A simple proportionality between the amplitude of the respiratory motor output (VT) and the respiratory period (TTOT) during such changes will not provide for regulation of arterial (PaCO2); the relationship requires a positive intercept of magnitude VD, i.e. VT=VATTOT+VD. We therefore determined the relationship between VT and TTOT when breathing frequency was changed in a ramp-like manner (from 6 to 20 cycles/min), in an imperceptible manner, during a paced-breathing protocol in which the subjects voluntarily triggered the breath onset, thereby imposing a rhythm different from the one spontaneously generated by the automatic central pattern generators (CPGs). While the resulting breath magnitude was strongly correlated to the breath duration (slope: 6.50+/-2.91 l/min) there was, in all cases, a statistically significant positive intercept on the VT axis (238+/-112 ml) leading to a relationship of the form: VT=VATTOT+VD. Consequently, the ventilatory output changed as a function of the breathing frequency-induced dead space ventilation changes, maintaining end-tidal PCO2 (PETCO2) constant. These results are consistent with a centrally set program for generating regulatory combinations of respiratory cycle durations and magnitudes that "take into account" the f-induced variation of dead space ventilation. This appears not to be dependent on the structures producing the respiratory rhythm (cortex versus central pattern generators). It is suggested that, during volitional control of breathing rhythm, the signal used for adjusting the magnitude to the timing of the ventilatory output is derived from information contained in the duration of preceding expiration.
当呼吸频率改变时,通气控制系统是否会根据生理死腔通气(VD)的调节需求来调整总通气量?如果是,又是如何调整的?在这种变化过程中,呼吸运动输出幅度(VT)与呼吸周期(TTOT)之间的简单比例关系无法调节动脉血二氧化碳分压(PaCO2);这种关系需要一个大小为VD的正截距,即VT = VATTOT + VD。因此,我们在一项定频呼吸方案中,以一种难以察觉的、类似斜坡的方式(从6次/分钟增加到20次/分钟)改变呼吸频率时,确定了VT与TTOT之间的关系。在该方案中,受试者自主触发呼吸起始,从而形成一种与自动中枢模式发生器(CPG)自发产生的节律不同的节律。虽然由此产生的呼吸幅度与呼吸持续时间密切相关(斜率:6.50±2.91升/分钟),但在所有情况下,VT轴上都存在统计学上显著的正截距(238±112毫升),从而得出如下形式的关系:VT = VATTOT + VD。因此,通气输出随呼吸频率引起的死腔通气变化而变化,维持呼气末二氧化碳分压(PETCO2)恒定。这些结果与一个中央设定程序一致,该程序用于生成呼吸周期持续时间和幅度的调节组合,“考虑”了频率诱导的死腔通气变化。这似乎不依赖于产生呼吸节律的结构(皮层与中枢模式发生器)。有人提出,在对呼吸节律进行自主控制期间,用于根据通气输出的时间调整幅度的信号源自前一次呼气持续时间中包含的信息。