Gautier H, Bonora M, Gaudy J H
Respir Physiol. 1986 Aug;65(2):181-96. doi: 10.1016/0034-5687(86)90049-6.
In conscious intact cats, oxygen breathing for up to 1 h does not modify ventilation, and the ventilatory response to CO2 in hyperoxia is not consistently decreased. However, oxygen breathing induces sustained hyperventilation in conscious cats after carotid body denervation. In anesthetized cats, oxygen breathing provokes a hypoventilation which is transient under light anesthesia but more sustained under deeper levels of anesthesia. At all levels of anesthesia, the ventilatory response to CO2 is decreased in hyperoxia as compared with normoxia. These results suggest that: the effects of hyperoxia include a central stimulating component, seen only in conscious animals, which offsets the decreased ventilatory drive from peripheral chemoreceptors; this central component is sensitive to anesthesia, thus allowing an explanation for the permanent decrease in ventilation and decrease in ventilatory response to CO2 observed when oxygen is given during deep anesthesia; and anesthesia may help to purposefully unmask factors involved in the control of breathing, but it markedly alters the normal functioning of the respiratory network.
在清醒且完整的猫中,呼吸氧气长达1小时不会改变通气,并且在高氧环境下对二氧化碳的通气反应并非持续降低。然而,在颈动脉体去神经支配后的清醒猫中,呼吸氧气会诱发持续的通气过度。在麻醉的猫中,呼吸氧气会引发通气不足,在浅麻醉状态下这种通气不足是短暂的,但在更深麻醉水平下则更持久。在所有麻醉水平下,与常氧相比,高氧环境下对二氧化碳的通气反应都会降低。这些结果表明:高氧的影响包括一个仅在清醒动物中出现的中枢刺激成分,它抵消了外周化学感受器导致的通气驱动力下降;这个中枢成分对麻醉敏感,这就解释了在深度麻醉期间给予氧气时观察到的通气永久性下降以及对二氧化碳的通气反应降低;并且麻醉可能有助于有目的地揭示参与呼吸控制的因素,但它会显著改变呼吸网络的正常功能。