Millhorn D E, Eldridge F L, Waldrop T G
Respir Physiol. 1980 Jul;41(1):87-103. doi: 10.1016/0034-5687(80)90025-0.
The inspiratory responses to stimulation by peripheral chemoreceptor, central chemoreceptor and calf muscle afferents were studied in anesthetized, or decerebrate, paralyzed cats whose end-tidal PCO2 was servo-controlled and kept constant. All stimuli were associated with immediate increases of inspiratory (phrenic) activity and at offset were followed by a respiratory afterdischarge lasting approximately five minutes. The level of inspiratory activity following decay of the afterdischarge was the same as the prestimulation control after central chemoreceptor and calf muscle stimulation. However, after peripheral chemoreceptor afferent stimulation the stable level of inspiratory activity following the afterdischarge had increased over the prestimulation level and remained elevated for as long as it was followed, up to 90 min. Decerebration, vagotomy, and section of the spinal cord at C--T1 did not prevent this long-lasting increase in respiration. We conclude that we have demonstrated a new ponto-medullary neural mechanism which is uniquely activated by peripheral chemoreceptor afferent input; once activated, this mechanism sustains respiration at an increased level for a long period of time.
在麻醉、去大脑或瘫痪的猫身上,研究了外周化学感受器、中枢化学感受器和小腿肌肉传入神经刺激引起的吸气反应,这些猫的呼气末PCO2通过伺服控制保持恒定。所有刺激均与吸气(膈神经)活动立即增加相关,刺激停止后伴有持续约五分钟的呼吸后放电。中枢化学感受器和小腿肌肉刺激后,后放电衰减后的吸气活动水平与刺激前对照相同。然而,外周化学感受器传入神经刺激后,后放电后的吸气活动稳定水平高于刺激前水平,并在长达90分钟的观察期内一直保持升高。去大脑、迷走神经切断和C-T1脊髓横断并不能阻止这种呼吸的长期增加。我们得出结论,我们已经证明了一种新的脑桥-延髓神经机制,该机制由外周化学感受器传入输入独特激活;一旦激活,该机制会在较长时间内维持呼吸在升高水平。