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目的:研究N-甲基-D-天门冬氨酸(NMDA)受体机制在动脉压力反射中的作用。方法:头端延髓腹外侧区(RVLM)前交感神经元(presympathetic neuron)与动脉压力反射相关,它们可被电刺激主动脉神经或升高动脉血压所抑制,其自发放电具有心性节律。根据这一特性,本研究用电生理学方法在17只雄性SD大鼠鉴定了27个假想的(putative)RVLM前交感神经元。以这些神经元对电刺激主动脉神经的反应为指标,观察在同侧孤束核(NTS)或尾端延髓腹外侧区(CVLM)微注射选择性NMDA受体拮抗剂CPP(0.1μL,50mmol/L)的作用。结果:在NTS微注射CPP可完全阻断或减弱电刺激主动脉神经引起的神经元抑制,但血压升高引起的神经元抑制不能完全被消除,神经元放电的心性节律仍然存在;在CVLM,CPP不仅完全阻断电刺激主动脉神经引起的神经元抑制,而且阻断血压升高引起的神经元抑制,神经元放电的心性节律消失。结论:NMDA受体机制在动脉压力反射中起着重要的介导作用;单侧孤束核的压力敏感神经元向单侧RVLM投射。
Objective: To investigate the role of N-methyl-D-aspartate (NMDA) receptor in arterial pressure reflex. Methods: The presympathetic neuron of RVLM was associated with arterial pressure reflex, which was inhibited by electrical stimulation of aorta nerve or elevated arterial blood pressure, and had spontaneous discharge with a cardiac rhythm. Based on this characteristic, 27 putative RVLM presympathetic neurons were identified in 17 male SD rats electrophysiologically. The responses of these neurons to electrical stimulation of aortic nerve were used as indices to observe the effects of selective NMDA receptor antagonist CPP (0.1 μL, 50 mmol) on the ipsilateral nucleus tractus solitarius (NTS) or caudal ventrolateral medulla (CVLM) / L) role. RESULTS: Microinjection of CPP into NTS could completely block or attenuate the neuronal inhibition induced by electrical stimulation of aortic nerve. However, the inhibition of neuron caused by high blood pressure can not be completely eliminated, and the cardiac rhythm of neuronal discharge still exists. In CVLM, CPP not only completely blocked the electrical stimulation of aortic nerve-induced neuronal suppression, but also blocked the elevation of blood pressure caused by neuronal inhibition, neuronal discharge rhythm disappeared. CONCLUSION: The NMDA receptor mechanism plays an important mediating role in arterial pressure reflex. The pressure-sensitive neurons of unilateral solitary bundle nucleus project to unilateral RVLM.