Panneton W M
Department of Anatomy and Neurobiology, St. Louis University School of Medicine, MO.
J Auton Nerv Syst. 1990 Jul;30(3):253-63. doi: 10.1016/0165-1838(90)90257-j.
Respiration was disrupted and bradycardia induced in anesthetized muskrats by stimulating the nasal cavity with a stream of either water or various concentrations of ammonia vapors. When responses induced by either ammonia or water were compared, ammonia vapors were considered preferable because the responses could be maintained reliably through relatively rapid periods of stimulation, and the post-stimulus recovery of heart rate and respiration was more predictable. Moreover, the bradycardia induced in the first 5 s of stimulation by dilutions of ammonia vapors was graded. After injections of lidocaine were made into the nucleus tractus solitarius a profound bradycardia to ammonia stimulation persisted despite disruption of normal respiratory rhythms and an inhibition of the baroreceptor reflex induced by phenylephrine administration. These results show that ammonia vapors stimulating the nasal chambers effectively elicit cardio-respiratory adjustments in anesthetized muskrats and that the bradycardia may be controlled by varying the intensity of the peripheral stimulus. The trigeminal contribution for this is emphasized since the bradycardia persists after reversible blockade of the solitary complex. These data suggest that the trigeminal input to cardiac motorneurons is via relatively few synapses and is over circuits which run parallel to those modulating cardiac activity in response to chemoreceptors, baroreceptors and pulmonary afferent fibers.
通过用一股水流或各种浓度的氨气刺激麻醉的麝鼠鼻腔，可导致呼吸紊乱和心动过缓。当比较氨气和水所引发的反应时，氨气被认为更可取，因为通过相对快速的刺激期能够可靠地维持反应，且刺激后心率和呼吸的恢复更可预测。此外，氨气稀释液在刺激的前5秒所引发的心动过缓呈分级状态。向孤束核注射利多卡因后，尽管正常呼吸节律被破坏且苯肾上腺素给药诱导的压力感受器反射受到抑制，但对氨气刺激仍持续出现深度心动过缓。这些结果表明，刺激鼻腔的氨气能有效引发麻醉麝鼠的心肺调节，且心动过缓可能通过改变外周刺激的强度来控制。由于在孤束复合体可逆性阻断后心动过缓仍持续，因此强调了三叉神经的作用。这些数据表明，三叉神经向心脏运动神经元的输入通过相对较少的突触，且是通过与那些响应化学感受器、压力感受器和肺传入纤维调节心脏活动的回路并行的回路。
