Tonic sympathetic chemoreflex after blockade of respiratory rhythmogenesis in the rat
Tonic sympathetic chemoreflex after blockade of respiratory rhythmogenesis in the rat
复制标题
DOI：
10.1113/jphysiol.1996.sp021263
复制
发表时间：
1996-03-15
影响因子：
5.5
通讯作者：
Guyenet, PG
中科院分区：
文献类型：
--
作者：
Koshiya, N;Guyenet, PG
1.我们试图确定刺激颈动脉化学感受器引起的交感神经放电(SND)增加是否需要参与呼吸节律和模式产生的延髓腹外侧部结构的完整性。实验是在乌拉坦麻醉、迷走神经切断、主动脉去传入、通风的大鼠身上进行的，除非有特殊情况(见第3段)。短暂低氧(N-2供S 5-12)或静脉注射NaCN(50-100mg·kg~(-1))可引起与膈神经放电同步的阵发性SND。对化学去传入的大鼠无影响。在未麻醉的迷走神经切断去大脑的大鼠，结扎颈内动脉保留了外周化学感受器功能，但取消了压力反射。在这种准备中，刺激外周化学感受器(2-6 S的N-2)也激活了与PND.同步的爆发的SND。双侧延髓腹外侧腹外侧区(CVLM)微量注射GABA(A)受体激动剂Muscimol即刻阻断交感压力感受性反射，消除静息和化学感受器刺激时的PND，但不改变化学感受器刺激产生的SND的平均增加。对化学感受器刺激反应的交感神经活动在1-13分钟后变得紧张性，并且仍然完全依赖于颈动脉窦神经的完整性。在静息状态和化学感受器刺激过程中，注射蝇草醇均可立即消除第X和第XII脑神经的呼吸流出。麝香酚消除了延髓头端腹外侧区神经元的开关呼吸模式。在化学感受器刺激期间，这些细胞被强直地激活或抑制。注射麝香酚可增加RVLM内血管运动交感前细胞的静息放电率，阻断压力感受器传入，但不改变化学感受器刺激对其兴奋的幅度。注射用蝇草酚消除了它们对呼吸的调节作用。总之，对化学感受器刺激的交感反应可能是由于两个过程的汇聚和整合：对RVLM神经元的非呼吸兴奋性输入和通过来自前Botzinger复合体的输入对其活动的呼吸模式。
1. We sought to determine whether the increase in sympathetic nerve discharge (SND) caused by carotid chemoreceptor stimulation requires the integrity of ventrolateral medullary structures involved in generating respiratory rhythm and pattern. Experiments were done in urethane-anaesthetized, vagotomized, aortic deafferented, ventilated rats except when indicated (see paragraph 3).2. Brief hypoxia (N-2 for 5-12 s) or I.V. NaCN (50-100 mu g kg(-1)) activated SND in bursts synchronized with the phrenic nerve discharge (PND). No effect was produced in chemodeafferented rats.3. In unanaesthetized vagotomized decerebrated rats, ligation of the internal carotid arteries preserved peripheral chemoreceptor function but abolished baroreflexes. In this preparation, stimulation of peripheral chemoreceptors (N-2 for 2-6 s) also activated SND in bursts synchronized with PND.4. Bilateral microinjection of the GABA(A) receptor agonist muscimol into the caudal ventrolateral medulla (CVLM) instantly blocked the sympathetic baroreflex, eliminated PND at rest and during chemoreceptor stimulation but did not change the mean increase in SND produced by chemoreceptor stimulation. Sympathoactivation in response to chemoreceptor stimulation became tonic after 1-13 min and was still totally dependent on the integrity of the carotid sinus nerves.5. Muscimol injection instantly eliminated the respiratory outflow of the Xth and XIIth cranial nerves, both at rest and during chemoreceptor stimulation.6. Muscimol eliminated the on-off respiratory pattern of neurons in the rostral ventrolateral medulla (RVLM). During chemoreceptor stimulation, these cells became activated or inhibited tonically.7. Muscimol injection raised the resting discharge rate of vasomotor presympathetic cells in RVLM, blocked their baroreceptor inputs but did not change the magnitude of their excitation by chemoreceptor stimulation. Muscimol injection eliminated their respiratory modulation.8. In conclusion, the sympathetic response to chemoreceptor stimulation may be due to convergence and integration in RVLM of two processes: respiration-independent excitatory input to RVLM neurons and respiratory patterning of their activities via inputs from the pre-Botzinger complex.