Forster H V, Klein J P, Hamilton L H, Kampine J P
J Appl Physiol Respir Environ Exerc Physiol. 1982 Feb;52(2):287-94. doi: 10.1152/jappl.1982.52.2.287.
This study was designed to determine whether 1) arterial PCO2 (PaCO2) increases when inspired PCO2 (PICO2) is increased from less than 0.4 Torr (eupnea) to 7 or 14 Torr, and 2) ventilatory sensitivity to CO2 (delta VE/ delta PaCO2) is greater at low levels of PICO2 (7-21 Torr) than it is at higher levels (28-42 Torr). Human subjects were studied while seated in an environmental chamber that permitted alteration of PICO2 by changing the chamber PCO2. In study 1, arterial blood was sampled over the final 5 min of a eupneic period and again 10-15 min later when PICO2 was 7 or 14 Torr. With this protocol, PACO2 was increased above eupnea by 0.7 (P less than 0.02) and 0.9 Torr (P less than 0.01) when PICO2 was 7 and 14 Torr, respectively. In study 2, arterial blood was sampled every 5 min during two 1-h periods of eupnea that were separated by 3 h during which PICO2 was increased by 7 Torr each 0.5 h. With this protocol there was no consistent difference in PACO2 between eupneic periods and periods when PICO2 was 7-14 Torr. There was a progressively increased hypercapnia as PICO2 was increased from 7 to 42 Torr. The delta VE/ delta PaCO2 was less than half for data obtained at low relative to high PICO2. The two studies demonstrated that measurement error and physiologic variation necessitate using a "powerful" experimental design (study 1) to detect small increases in PaCO2. On the basis of these results, we have concluded that there is no apparent reason to postulate a sensory mechanism other than the carotid and intracranial chemoreceptors to account for the hyperpnea during CO2 inhalation. Specifically, isocapnic hyperpnea probably does not occur.
1）当吸入二氧化碳分压（PICO2）从低于0.4托（平静呼吸）增加到7或14托时，动脉血二氧化碳分压（PaCO2）是否会升高；2）在低水平PICO2（7 - 21托）时，通气对二氧化碳的敏感性（δVE/δPaCO2）是否高于高水平（28 - 42托）。研究对象为人类受试者，他们坐在一个环境舱中，通过改变舱内二氧化碳分压来改变PICO2。在研究1中，在平静呼吸期的最后5分钟采集动脉血样，10 - 15分钟后当PICO2为7或14托时再次采集。采用该方案，当PICO2为7托和14托时，肺泡二氧化碳分压（PACO2）分别比平静呼吸时升高了0.7（P < 0.02）和0.9托（P < 0.01）。在研究2中，在两个1小时的平静呼吸期内，每隔5分钟采集一次动脉血样，这两个平静呼吸期间隔3小时，在此期间PICO2每0.5小时升高7托。采用该方案，平静呼吸期与PICO2为7 - 14托的时期之间，PACO2没有一致的差异。随着PICO2从7托增加到42托，高碳酸血症逐渐加重。相对于高PICO2时获得的数据，低PICO2时获得的数据的δVE/δPaCO2不到其一半。这两项研究表明，测量误差和生理变异使得有必要采用“有力的”实验设计（研究1）来检测PaCO2的微小升高。基于这些结果，我们得出结论，除了颈动脉和颅内化学感受器外，没有明显理由假定存在其他感觉机制来解释吸入二氧化碳期间的呼吸急促。具体而言，等碳酸性呼吸急促可能不会发生。
