Nishino T, Yonezawa T, Honda Y
Anesthesiology. 1981 Sep;55(3):286-91. doi: 10.1097/00000542-198109000-00018.
In order to study the effects of PaCO2 and PaO2 on the laryngeal closure reflex, changes in laryngeal resistance of the isolated cat larynx were measured before and during the stimulation of the superior laryngeal nerve (SLN) at various levels of PaCO2 and PaO2. The results showed that laryngeal resistance before SLN stimulation [LR (baseline)] increased slightly during hypocapnia. SLN stimulation produced laryngospasm which was defined as a sharp rise in the laryngeal resistance. Hypercapnia alone and hypoxia alone increased ventilation but decreased the degree and duration of laryngospasm due to SLN stimulation. On the other hand, hypocapnia augmented and prolonged the duration of this laryngospasm. These results suggest that PaCO2 and PaO2 regulate the laryngeal closure reflex in a way such that the degree of laryngospasm changes in inverse proportion to the activity of the respiratory center.
为了研究动脉血二氧化碳分压(PaCO2)和动脉血氧分压(PaO2)对喉关闭反射的影响,在不同PaCO2和PaO2水平下,于刺激喉上神经(SLN)之前及期间,测量离体猫喉的喉阻力变化。结果显示,在低碳酸血症期间,SLN刺激前的喉阻力[LR(基线)]略有增加。SLN刺激引发喉痉挛,其定义为喉阻力急剧上升。单纯高碳酸血症和单纯低氧血症均可增加通气,但会降低因SLN刺激引起的喉痉挛程度和持续时间。另一方面,低碳酸血症会增强并延长这种喉痉挛的持续时间。这些结果表明,PaCO2和PaO2以某种方式调节喉关闭反射,使得喉痉挛程度与呼吸中枢活动呈反比变化。