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

将N-甲基-D-天冬氨酸（NMDA）微量注射到麻醉、麻痹和人工通气大鼠的孤束核（NTS）内，并用标记微球测定脑血流量（CBF）。刺激孤束核同侧大脑皮质CBF显著降低（P<0.01）（n=9）。刺激孤束核同侧大脑皮层脑血管阻力（CVR）显著增加（P<0.01）。阻断孤束核内NMDA受体可消除孤束核内注射NMDA引起的CBF降低和CVR升高反应（n=9）。阻断NTS中的非NMDA受体对CBF降低和CVR增加反应几乎没有影响（n=10）。在延髓腹外侧降压区（VLDA）内微量注射L-谷氨酸（1.7nmol），可使刺激侧大脑皮质CBF显著降低（P<0.01），CVR显著增加（P<0.01）。颈交感神经切除术阻断了化学刺激VLDA引起的CBF下降和CVR增加（n=10）。延髓腹外侧加压区（VLPA）内微量注射蝇蕈醇（muscimol）抑制VLPA神经元，可阻断化学刺激VLDA（n=11）引起的CBF降低和CVR升高反应。这些结果表明，血管收缩通路，以控制脑血管涉及兴奋性投射从VLDA的VLPA和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.