Gautier H, Bonora M, Zaoui D
Atelier de Physiologie Respiratoire, Faculté de Médecine Saint Antoine, Paris, France.
J Appl Physiol (1985). 1990 Oct;69(4):1423-8. doi: 10.1152/jappl.1990.69.4.1423.
To clarify the mechanisms involved in the ventilatory response to the inhalation of low concentrations of CO (0.18-0.22% in air), the roles of the arterial chemoreceptors and the forebrain structures have been investigated in unanesthetized adult cats. The ventilatory response was observed in conscious animals intact, after carotid denervation (CD), and after midcollicular decerebration. The results show that the initial small ventilatory depression was unaffected by CD but that the subsequent characteristic tachypnea was blunted after CD even after more prolonged exposure to CO. The CO tachypnea was not observed after decerebration, but a residual hyperventilation was noted with the higher concentration used. It may be concluded that carotid chemoreceptors do not mediate the CO tachypnea, which may then originate in suprapontine structures as shown by comparison of intact and decerebrate animals. The blunting of the tachypnea after CD may be caused by the relative hypercapnia observed in CD animals. The residual hyperventilation observed in decerebrate animals may be caused by central acidosis and/or some peripheral potentiation of chemoreceptor activity resulting from the decrease in arterial blood pressure that accompanied CO inhalation in decerebrate animals.
为了阐明吸入低浓度一氧化碳（空气中含量为0.18 - 0.22%）时通气反应所涉及的机制，在未麻醉的成年猫中研究了动脉化学感受器和前脑结构的作用。在清醒且完整的动物、颈动脉去神经支配（CD）后以及中脑丘间去大脑后观察通气反应。结果表明，最初的小幅度通气抑制不受CD影响，但随后典型的呼吸急促在CD后变钝，即使在更长时间暴露于一氧化碳后也是如此。去大脑后未观察到一氧化碳所致的呼吸急促，但在使用较高浓度时注意到有残余的过度通气。可以得出结论，颈动脉化学感受器不介导一氧化碳所致的呼吸急促，通过完整动物和去大脑动物的比较表明，呼吸急促可能起源于脑桥上结构。CD后呼吸急促变钝可能是由于在CD动物中观察到的相对高碳酸血症所致。在去大脑动物中观察到的残余过度通气可能是由中枢性酸中毒和/或去大脑动物吸入一氧化碳时伴随的动脉血压下降导致的化学感受器活动的某种外周增强所致。
