Blanco C E, Hanson M A, Johnson P, Rigatto H
J Appl Physiol Respir Environ Exerc Physiol. 1984 Jan;56(1):12-7. doi: 10.1152/jappl.1984.56.1.12.
In 19 pentobarbital sodium-anesthetized kittens aged 5-34 days, inspired O2 was reduced from 21 to 6-12%. Respiratory frequency (f) and tidal volume (VT) increased within 30 s. Over 5 min f fell to about 60% below control; VT usually fell but remained above control. Arterial pressure fell in 80% of trials, sometimes before f fell. Arterial CO2 was below control, but raising inspired CO2 to keep expired CO2 at control did not prevent the fall in f and VT. The relation between VT and esophageal pressure or diaphragm electromyogram (EMG) did not change consistently, nor was the ratio of high to low frequencies in the diaphragm EMG altered. Carotid chemoreceptor discharge increased within 15 s, and at 5 min it was much above control. We conclude that the change in the breathing pattern in hypoxia is probably due to the activation of a central mechanism.
在19只5 - 34日龄的戊巴比妥钠麻醉小猫中，吸入氧从21%降至6 - 12%。呼吸频率（f）和潮气量（VT）在30秒内增加。在5分钟内，f降至比对照低约60%；VT通常下降但仍高于对照。80%的试验中动脉压下降，有时在f下降之前。动脉二氧化碳低于对照，但提高吸入二氧化碳以使呼出二氧化碳保持在对照水平并不能防止f和VT下降。VT与食管压力或膈肌肌电图（EMG）之间的关系没有持续变化，膈肌EMG中高频与低频的比值也没有改变。颈动脉化学感受器放电在15秒内增加，在5分钟时远高于对照。我们得出结论，低氧时呼吸模式的改变可能是由于一种中枢机制的激活。
