Lahiri S, Mokashi A, Delaney R G, Fishman A P
Respir Physiol. 1978 Sep;34(3):359-75. doi: 10.1016/0034-5687(78)90134-2.
The PaO2 and PaCO2 stimulus thresholds for activity of carotid chemoreceptors and for ventilation were investigated in twenty anesthetized adult cats at sea level. Over the range studied PaCO2 threshold for carotid chemoreceptors decreased with increasing intensity of hypoxia showing stimulus interaction. Once begun, the carotid chemoreceptor activity increased gradually at a rate that was inversely related to initial PaO2. The greater the initial hypoxia the greater was the carotid chemoreceptor activity at which the first inspiration occurred, apnea was shorter and inspiratory PaCO2 threshold lower. Hypoxia per se depressed the central mechanism for the resumption of inspiration. We conclude that (1) carotid chemoreceptor PaO2-PaCO2 stimulus thresholds are largely interdependent; (2) these receptors are activated at a lower PaO2-PaCO2 stimulus strength than ventilation is; (3) an increased input from peripheral chemoreceptors initiates breathing at a lower PaCO2 indicating that central chemoreceptor threshold is lower than the PCO2 threshold for inspiration; (4) a finite total input from the receptors is needed to start ventilation.
在海平面条件下,对20只麻醉的成年猫的颈动脉化学感受器活动及通气的动脉血氧分压(PaO2)和动脉血二氧化碳分压(PaCO2)刺激阈值进行了研究。在所研究的范围内,颈动脉化学感受器的PaCO2阈值随缺氧强度增加而降低,显示出刺激相互作用。一旦开始,颈动脉化学感受器活动以与初始PaO2呈负相关的速率逐渐增加。初始缺氧程度越大,首次吸气时的颈动脉化学感受器活动越大,呼吸暂停越短,吸气时的PaCO2阈值越低。缺氧本身会抑制恢复吸气的中枢机制。我们得出结论:(1)颈动脉化学感受器的PaO2 - PaCO2刺激阈值在很大程度上相互依赖;(2)这些感受器在低于通气的PaO2 - PaCO2刺激强度时被激活;(3)外周化学感受器输入增加会在较低的PaCO2时启动呼吸,表明中枢化学感受器阈值低于吸气的PCO2阈值;(4)启动通气需要来自感受器的有限总输入。