Klein J P, Forster H V, Bisgard G E, Kaminski R P, Pan L G, Hamilton L H
J Appl Physiol Respir Environ Exerc Physiol. 1982 Jun;52(6):1614-22. doi: 10.1152/jappl.1982.52.6.1614.
The purpose of these studies was to gain insight into mechanisms regulating pulmonary ventilation (VE), arterial CO2 partial pressure (PaCO2), and arterial pH (pHa) in ponies when inspired CO2 partial pressure (PICO2) is above normal. Ponies were studied four times daily each weekday for 2 wk in an environmental chamber. Each study consisted of a 15-min control period (PICO2 = 0.7 Torr) followed by a 15- to 30-min experimental period during which PICO2 in the chamber was 0.7, 7, 14, 21, 28, or 42 Torr (PIO2 = 147 Torr throughout). Between 11 and 15 min of each period, four 3-ml samples of arterial blood were drawn, each over 45 s. In 12 normal ponies, elevation of PICO2 to 7 Torr caused PaCO2 to increase approximately 0.4 Torr (P less than 0.01) and pHa to decrease approximately 0.003 (P less than 0.02) relative to control. The hypercapnia and acidosis increased progressively as PICO2 was increased in 7- to 14-Torr increments to 42 Torr (P less than 0.02). Accordingly, the hyperpnea in these ponies during CO2 inhalation could have been mediated by carotid and intracranial chemoreceptors. One month after carotid body denervation (CBD) in nine ponies, PaCO2 during control conditions was 6 Torr above normal, but during CO2 inhalation, PaCO2 changed less from control than during CO2 inhalation before CBD (P less than 0.01). The delta VE/ delta PaCO2 near eupneic PaCO2 appeared to be above normal 1 mo after CBD (P less than 0.01). The mechanism of this increase was not discernible from our data. Finally, our data indicated that the magnitude of the hypercapnia and acidosis during CO2 inhalation was inversely related to PaCO2 and breathing frequency during control conditions.
这些研究的目的是深入了解当吸入二氧化碳分压（PICO2）高于正常水平时，调节小马肺通气量（VE）、动脉血二氧化碳分压（PaCO2）和动脉血pH值（pHa）的机制。在环境舱中，每个工作日对小马每天进行4次研究，持续2周。每次研究包括一个15分钟的对照期（PICO2 = 0.7托），随后是一个15至30分钟的实验期，在此期间舱内的PICO2为0.7、7、14、21、28或42托（整个过程中PIO2 = 147托）。在每个时期的11至15分钟之间，抽取4份3毫升的动脉血样本，每份样本采集时间为45秒。在12匹正常小马中，与对照相比，PICO2升高至7托会导致PaCO2增加约0.4托（P < 0.01），pHa降低约0.003（P < 0.02）。随着PICO2以7至14托的增量增加到42托，高碳酸血症和酸中毒逐渐加重（P < 0.02）。因此，这些小马在吸入二氧化碳期间的呼吸急促可能是由颈动脉和颅内化学感受器介导的。在9匹小马进行颈动脉体去神经支配（CBD）1个月后，对照条件下的PaCO2比正常水平高6托，但在吸入二氧化碳期间，PaCO2相对于CBD前吸入二氧化碳时的对照变化较小（P < 0.01）。在接近正常呼吸PaCO2时，CBD后1个月的ΔVE/ΔPaCO2似乎高于正常水平（P < 0.01）。从我们的数据中无法看出这种增加的机制。最后，我们的数据表明，吸入二氧化碳期间高碳酸血症和酸中毒的程度与对照条件下的PaCO2和呼吸频率呈负相关。
