Hanna B D, Lioy F, Polosa C
J Auton Nerv Syst. 1981 Apr;3(2-4):421-35. doi: 10.1016/0165-1838(81)90079-5.
In anesthetized, vagotomized, paralyzed, artificially ventilated cats with aortic nerves cut, we recorded the response of 28 sympathetic preganglionic neurons (SPNs) of the cervical sympathetic trunk of changes in arterial pCO2. We observed the effects on these responses of: (i) surgical denervation of carotid sinus chemoreceptors in normoxia (paO2 110 mm Hg); and (ii) hyperoxia (paO2 greater than 350 mm Hg) which is known to depress peripheral chemoreceptor sensitivity to CO2. Stimulus-response curves, obtained by rebreathing at constant paO2, were used to detect the effects of these manoeuvres. The present experiments have confirmed previous observations demonstrating the CO2-sensitivity of this neuron population. The population average firing rate, as a function of paCO2, describes a sigmoid curve, increasing continuously between 20 and 90 mm Hg and asymptotically approaching plateaus at the highest and lowest paCO2 values. Carotid sinus nerve section caused a decrease of the average response of the population at all paCO2 values, resulting in a displacement to the right of the response curve, in a decrease in slope and maximum values. On the assumption that the CO2 response curve after carotid sinus nerve section is due to central chemoreceptor input, and that there is a simple addition between the effects of central and carotid chemoreceptors, the difference between CO2 response curves ("difference curves") before and after denervation represents the contribution of the carotid chemoreceptors. A comparison of this "difference curve" with the curve obtained after denervation reveals that the contribution of the carotid chemoreceptors is of the same magnitude as that of the central chemoreceptors up to a paCO2 value of 60-70 mm Hg. Beyond this value, the carotid contribution declines and becomes a smaller component of the total response, whereas the contribution of the central chemoreceptors continues to increase. Similar results were obtained with rebreathing in hyperoxia, after correction for the central excitatory effect of hyperoxia. Hyperoxia never caused a depression of the CO2 response of units after section of the carotid sinus nerve. Observation of the effects of the two manoeuvres on individual SPNs leads to the conclusion that in approximately half of the CO2-sensitive units there is an overlap of central and peripheral chemoreceptor input. The remainder of the CO2-sensitive units receive input only from the central chemoreceptors.
在麻醉、切断迷走神经、麻痹并进行人工通气且切断主动脉神经的猫身上，我们记录了颈交感干28个交感神经节前神经元（SPN）对动脉血二氧化碳分压（pCO₂）变化的反应。我们观察了以下因素对这些反应的影响：（i）在常氧（动脉血氧分压[paO₂] 110 mmHg）条件下对颈动脉窦化学感受器进行手术去神经支配；以及（ii）高氧（paO₂大于350 mmHg），已知高氧会降低外周化学感受器对二氧化碳的敏感性。通过在恒定paO₂条件下进行重复呼吸获得刺激 - 反应曲线，以检测这些操作的效果。本实验证实了先前的观察结果，即证明了这群神经元对二氧化碳敏感。群体平均放电率作为paCO₂的函数，描绘出一条S形曲线，在20至90 mmHg之间持续增加，并在最高和最低paCO₂值时渐近地接近平稳状态。切断颈动脉窦神经导致在所有paCO₂值下群体的平均反应降低，导致反应曲线向右移位，斜率和最大值减小。假设切断颈动脉窦神经后的二氧化碳反应曲线是由于中枢化学感受器输入所致，并且中枢和颈动脉化学感受器的作用之间存在简单相加，那么去神经支配前后二氧化碳反应曲线（“差异曲线”）之间的差异代表了颈动脉化学感受器的贡献。将此“差异曲线”与去神经支配后获得的曲线进行比较发现，在paCO₂值达到60 - 70 mmHg之前，颈动脉化学感受器的贡献与中枢化学感受器的贡献大小相同。超过此值，颈动脉的贡献下降并成为总反应中较小的组成部分，而中枢化学感受器的贡献继续增加。在对高氧的中枢兴奋作用进行校正后，高氧重复呼吸也得到了类似结果。切断颈动脉窦神经后，高氧从未导致单位对二氧化碳反应的抑制。观察这两种操作对单个SPN的影响得出结论，在大约一半对二氧化碳敏感的单位中，存在中枢和外周化学感受器输入的重叠。其余对二氧化碳敏感的单位仅接受来自中枢化学感受器的输入。
