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

将N-甲基-D-天冬氨酸(NMDA)微量注射到乌拉坦麻醉、麻痹和人工呼吸大鼠的孤束核(NTS)，用标记微球测定脑血流量(CBF)。刺激NTS同侧大脑皮质脑血流量显著降低(P<0.01)。刺激NTS同侧大脑皮质脑血管阻力(CVR)显著增加(P<0.01)。阻断NTS内NMDA受体可阻断NTS内微量注射NMDA引起的CBF减少和CVR增加反应(n=9)。阻断NTS的非NMDA受体对CBF下降和CVR增加反应影响不大(n=10)。结果提示，孤束核内的N-甲基-D-天冬氨酸受体可能参与了脑循环的调控。延髓降压区腹外侧区微量注射L谷氨酸(1.7nmol)后，9只大鼠同侧大脑皮质的脑血流量显著降低(P<0.01)，脑血管阻力显著增加(P<0.01)。颈交感神经切断可阻断化学刺激VLDA引起的CBF下降和CVR增加(n=10)。延髓腹外侧加压区(VLPA)内微量注射蝇毒酚引起的神经元抑制可阻断化学刺激VLDA引起的CBF减少和CVR增加反应(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，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.