Jung R, Bruce E N, Katona P G
Department of Biomedical Engineering, School of Engineering, Case Western Reserve University, Cleveland, OH 44106.
Brain Res. 1991 Nov 15;564(2):286-95. doi: 10.1016/0006-8993(91)91465-d.
The role of caudal ventrolateral medullary (CVLM) depressor neurons in influencing arterial pressure and ventilation as well as the baroreflex control of arterial pressure was investigated, and the part played by excitatory N-methyl-D-aspartate (NMDA) and non-NMDA receptors in mediating the responses was determined. In urethane-anesthetized, spontaneously breathing rats unilateral microinjections into the caudal depressor area of the broad-band glutamatergic antagonist kynurenic acid (KYN, 5 nmol or 1.58 nmol), or NMDA antagonist 2-amino-5-phosphonovaleric acid (2-APV, 2.7 nmol), or the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 0.257 nmol) caused a respiratory arrest within 4 min and the animals had to be artificially ventilated. Respiratory frequency increased on injecting KYN and CNQX while it did not change significantly with 2-APV. Apnea resulted from progressive decrease in tidal volume. During the apnea ventilation with 5% CO2 did not revive breathing. Mean arterial pressure (MAP) increased significantly with KYN and 2-APV injections but not with CNQX. The baroreflex decrease of MAP, elicited by left or right aortic depressor nerve stimulation, was significantly reduced or abolished after bilateral microinjections of all 3 antagonists. Ventilation as well as the baroreflex usually recovered after 1-1.5 h. Microinjections of the same doses of antagonists into the facial nucleus, as well as application of KYN (25 nmol) to the ventral medullary surface above the hypoglossal rootlets, had no significant effect. The results support previous findings that the CVLM neurons of the rat inhibit sympathetic neurons providing the vasomotor tone, and that an intact CVLM is obligatory for mediating the baroreflex decrease of arterial pressure. The results also indicate that: (1) the CVLM is essential for sustaining ventilation in the rat; (2) only NMDA receptors are involved in maintaining baseline blood pressure while both NMDA and non-NMDA receptors mediate the baroreceptor depressor reflex; and (3) both NMDA and non-NMDA receptor activation is necessary to sustain ventilation.
研究了延髓尾端腹外侧（CVLM）降压神经元在影响动脉血压和通气以及动脉压力的压力感受性反射控制方面的作用，并确定了兴奋性N-甲基-D-天冬氨酸（NMDA）和非NMDA受体在介导这些反应中所起的作用。在氨基甲酸乙酯麻醉、自主呼吸的大鼠中，向尾端降压区单侧微量注射宽带谷氨酸能拮抗剂犬尿喹啉酸（KYN，5 nmol或1.58 nmol）、NMDA拮抗剂2-氨基-5-磷酸戊酸（2-APV，2.7 nmol）或非NMDA拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX，0.257 nmol），会在4分钟内导致呼吸停止，动物必须进行人工通气。注射KYN和CNQX时呼吸频率增加，而注射2-APV时呼吸频率无明显变化。呼吸暂停是由潮气量逐渐减少引起的。在呼吸暂停期间，用5%二氧化碳进行通气并不能恢复呼吸。注射KYN和2-APV后平均动脉压（MAP）显著升高，而注射CNQX后则无明显变化。通过刺激左或右主动脉降压神经引起的MAP压力感受性反射性降低，在双侧微量注射所有三种拮抗剂后显著降低或消失。通气以及压力感受性反射通常在1 - 1.5小时后恢复。向面神经核内微量注射相同剂量的拮抗剂，以及将KYN（25 nmol）应用于舌下神经根上方的延髓腹侧面，均无显著影响。这些结果支持了先前的研究发现，即大鼠的CVLM神经元抑制提供血管运动张力的交感神经元，并且完整的CVLM对于介导动脉压力的压力感受性反射性降低是必不可少的。结果还表明：（1）CVLM对于维持大鼠的通气至关重要；（2）只有NMDA受体参与维持基础血压，而NMDA和非NMDA受体均介导压力感受器降压反射；（3）NMDA和非NMDA受体的激活对于维持通气都是必要的。
