Gautier H
Respir Physiol. 1986 Jun;64(3):307-16. doi: 10.1016/0034-5687(86)90124-6.
The ventilatory response to CO hypoxia (FICO = 0.0025), hypercapnia, and hypoxia was studied in a group of intact, conscious cats before and during chronic administration of phenobarbital (60 mg/day). It was found that the ventilatory response to hypercapnia or hypoxia was not significantly modified during phenobarbital administration. However, the ventilatory response to CO hypoxia was markedly blunted with phenobarbital: the initial ventilatory inhibition was still observed but the subsequent hyperventilation was delayed. Furthermore, the tachypnea was less intense and the decrease in tidal volume was smaller during CO hypoxia. In addition, the behavioral reactions which usually accompanied the tachypnea were attenuated and unconsciousness was often noted. These results indicate that the modifications caused by phenobarbital do not result from a general inhibition of the respiratory control network but rather from a selective inhibition of the structures rostral to the brain stem. As a consequence, the behavioral reactions and resulting respiratory activation were attenuated. Since the hypoxic tachypnea and behavioral reactions are observed only during central hypoxemia, it is concluded that arterial chemoreceptor afferents normally inhibit the supra-pontine structures which are otherwise stimulated by central hypoxemia.
在一组完整、清醒的猫中，于长期给予苯巴比妥（60毫克/天）之前及期间，研究了对一氧化碳性缺氧（FICO = 0.0025）、高碳酸血症和缺氧的通气反应。结果发现，在给予苯巴比妥期间，对高碳酸血症或缺氧的通气反应无显著改变。然而，苯巴比妥使对一氧化碳性缺氧的通气反应明显减弱：仍可观察到最初的通气抑制，但随后的过度通气延迟。此外，在一氧化碳性缺氧期间，呼吸急促程度较轻，潮气量下降较小。另外，通常伴随呼吸急促的行为反应减弱，且常出现意识丧失。这些结果表明，苯巴比妥引起的改变并非源于对呼吸控制网络的全面抑制，而是源于对脑干以上结构的选择性抑制。因此，行为反应及由此产生的呼吸激活减弱。由于仅在中枢性低氧血症期间观察到低氧性呼吸急促和行为反应，所以得出结论：动脉化学感受器传入神经通常抑制桥脑以上结构，而这些结构在其他情况下会受到中枢性低氧血症的刺激。
