Trzebski A, Kubin L
J Auton Nerv Syst. 1981 Apr;3(2-4):401-20. doi: 10.1016/0165-1838(81)90078-3.
Out of 27 cats anesthetized with chloralose-urethane mixture, paralyzed, vagotomized and artificially ventilated, phrenic nerve response to systemic hypercapnia (7-8 vol.% CO2/O2 mixture) was accompanied by an increase in blood pressure and sympathetic discharge in 19 cats. Out of these 19 cats, 12 were totally debuffered and in the remaining 7 cats one carotid sinus nerve was left intact. Single unit activity in the sympathetic cervical nerve and spontaneous mass activity in the cervical, splanchnic, renal sympathetic and phrenic nerves were recorded. Evoked response in the phrenic nerve was produced by electrical stimulation of the descending bulbospinal inspiratory pathways in the midplane area of the medulla or in the ventrolateral cervical spinal cord. Starting from the control mean end-tidal CO2 concentration of 4.7 vol.% (+/- 1.0 S.D.) a progressing hypocapnia was induced by hyperventilation up to the end-tidal CO2 concentration of 1.3-3.2 vol.% (mean 2.4 vol.% +/- 0.5 S.D.) significantly below paCO2 apneic threshold. In chemo- and baroreceptor denervated cats with a pressor and excitatory sympathetic response to hypercapnia, a hypocapnia resulted in a fall of the arterial blood pressure (mean 16.9 mm Hg +/- 7.5 S.D., 2.2 kpa +/- S.D.). With the increasing paCO2 over the period of hypocapnic apnea a pressor and excitatory sympathetic response preceded, in all experiments, the onset of the phrenic nerve rhythmic activity. The difference between paCO2 threshold for the pressor and sympathetic response (35.7 mm Hg +/- 3.6 S.D., 4.7 kpa +/- 0.5 S.D.) and paCO2 threshold for the reappearance of the phrenic nerve rhythmic activity (43.6 mm Hg +/- 2.6 S.D., 5.8 kpa +/- 0.3 S.D.) was highly significant. If apneic hypocapnia was combined with the continuous stimulation of the afferent fibers of the superior laryngeal nerve the CO2 threshold for phrenic rhythmic activity was significantly increased whereas CO2 threshold for the pressor and sympathetic excitatory response remained unchanged. CO2 administration during hypocapnia apnea caused a progressing reduction of the magnitude of the evoked phrenic nerve response. From these findings it is concluded that the central excitatory effect of CO2 on the sympathetic activity may be accomplished in the absence of the rhythmic respiratory activity and independently of the subthreshold tonic inspiratory activity. Pressor and sympathetic excitatory response to CO2 observed during hypocapnic apnea is presumably caused by a neuronal pool different from that responsible for the central inspiratory activity. It is suggested that this CO2 sensitive neuronal mechanism might be involved in the central generation of sympathetic tone.
在27只使用水合氯醛 - 乌拉坦混合物麻醉、麻痹、切断迷走神经并进行人工通气的猫中，19只猫的膈神经对全身性高碳酸血症（7 - 8体积％CO₂/O₂混合物）的反应伴随着血压升高和交感神经放电增加。在这19只猫中，12只完全去除缓冲神经，其余7只猫保留一条完整的颈动脉窦神经。记录了颈交感神经的单单位活动以及颈、内脏、肾交感神经和膈神经的自发群体活动。膈神经的诱发反应通过电刺激延髓中平面区域或颈脊髓腹外侧的下行延髓脊髓吸气通路产生。从控制时的平均呼气末CO₂浓度4.7体积％（±1.0标准差）开始，通过过度通气诱导逐渐降低的低碳酸血症，直至呼气末CO₂浓度降至1.3 - 3.2体积％（平均2.4体积％±0.5标准差），显著低于动脉血二氧化碳分压（PaCO₂）的呼吸暂停阈值。在化学感受器和压力感受器去神经支配的猫中，对高碳酸血症有升压和兴奋性交感反应，低碳酸血症导致动脉血压下降（平均16.9毫米汞柱±7.5标准差，2.2千帕±标准差）。在低碳酸血症呼吸暂停期间，随着PaCO₂的升高，在所有实验中，升压和兴奋性交感反应先于膈神经节律性活动的开始。升压和交感反应的PaCO₂阈值（35.7毫米汞柱±3.6标准差，4.7千帕±0.5标准差）与膈神经节律性活动再次出现的PaCO₂阈值（43.6毫米汞柱±2.6标准差，5.8千帕±0.3标准差）之间的差异非常显著。如果呼吸暂停性低碳酸血症与持续刺激喉上神经的传入纤维相结合，膈神经节律性活动的CO₂阈值会显著升高，而升压和交感兴奋反应的CO₂阈值保持不变。在低碳酸血症呼吸暂停期间给予CO₂会导致诱发膈神经反应的幅度逐渐降低。从这些发现可以得出结论，CO₂对交感神经活动的中枢兴奋作用可能在没有节律性呼吸活动且独立于阈下紧张性吸气活动的情况下实现。在低碳酸血症呼吸暂停期间观察到的对CO₂的升压和交感兴奋反应可能是由与负责中枢吸气活动的神经元池不同的神经元池引起的。有人认为这种对CO₂敏感的神经元机制可能参与交感神经紧张性的中枢产生。
