Brain stem pathway to control cerebral circulation from nucleus tractus solitarii and its neurotransmitter

将n -甲基- d -天冬氨酸（NMDA）微注射到聚氨酯麻醉、麻痹和人工通气大鼠的孤立束核（NTS）中，并用标记微球联合测定脑血流量（CBF）。受刺激的NTS同侧大脑皮层CBF明显减少（P<0.01） （n=9）。受刺激的NTS同侧大脑皮层脑血管阻力（CVR）显著升高（p<0.01）。阻断NMDA受体可以消除NMDA微注射引起的CBF减少和CVR增加的反应（n=9）。阻断NTS中非nmda受体对CBF降低和CVR增加反应的影响很小（n=10）。这些结果提示NTS中的NMDA受体可能参与脑循环的控制。l -谷氨酸（1.7nmol）微注射于腹外侧髓质抑制区（VLDA）后，脑CBF显著（p<0.01）降低，VLDA刺激侧同侧大脑皮质CVR显著（p<0.01）升高（n=9）。颈交感神经切除术阻断了VLDA化学刺激引起的CBF下降和CVR增加（n=10）。向腹外侧延髓加压区（VLPA）微注射muscimol可抑制VLDA化学刺激后CBF减少和CVR增加的反应（n=11）。这些结果表明，控制脑血管的血管收缩通路涉及从VLDA到VLPA的兴奋性投射，并且脑循环的变化是由颈交感神经介导的。

N-methyl-D-aspartic acid (NMDA) was microinjected into the nucleus tractus solitarii (NTS) of urethane-anesthetized, paralyzed and artificially ventilated rats, and cerebral blood flow (CBF) was determined using a combination of labeled microspheres. The CBF in the cerebral cortex ipsilateral to the stimulated NTS significantly (P<0.01) decreased (n=9). The cerebrovascular resistance (CVR) in the cerebral cortex ipsilateral to the stimulated NTS significantly (p<0.01) increased. Blockade of NMDA receptors in the NTS abolished the CBF decrease and CVR increase responses elicited by microinjection of the NMDA into the NTS (n=9). Blockade of non-NMDA receptors in the NTS had little effect on the CBF decrease and CVR increase responses (n=10). These results suggest that the NMDA receptors in the NTS may be involved in the control of cerebral circulation.Microinjection of L-glutamate (1.7nmol) into the ventrolateral medullary depressor area (VLDA) produced a significant (p<0.01) decrease in CBF and significant (P<0.01) increase in CVR in the cerebral cortex ipsilateral to the stimulated VLDA side (n=9). Cervical sympathectomy blocked the decrease in CBF and increase in CVR elicited by chemical stimulation of the VLDA (n=10). Depression of the ventrolateral medullary pressor area (VLPA) neurons induced by microinjection of muscimol into the VLPA blocked the CBF decrease and CVR increase responses following chemical stimulation of VLDA (n=11). These results suggest that a vasoconstrictor pathway to control cerebral vessels involves an excitatory projection from the VLDA to the VLPA and the changes in cerebral circulation are mediated by the cervical sympathetic nerves.