Study on pathophysiology of central nervous system in neurogenic pulmonary edema (role of vagal nerve and nitric oxide)

1.观察单侧迷走神经切断2周和4周对纤维蛋白性肺水肿发生率及延髓一氧化氮合酶表达的影响。(1)We提出左迷走神经切断术后2周，孤束核中一氧化氮的增加可能对神经源性肺水肿的发展具有抑制作用。（2）切断左侧迷走神经4周后，上述变化不明显。（2）脑池内注射L-谷氨酸（L-Glu），通过NMDA受体促进神经末梢释放NO，探讨NO在神经源性肺水肿中的作用。（1）左侧迷走神经切断后2周，NMDAR 1仅在孤束核表达，NO含量与L-Glu含量成正比增加。（2）脑池内注射L-Glu可降低纤维蛋白诱导的肺水肿的发生率和肺湿重。（3）L-Glu的这种抑制作用在L-NAME和MK 0 -801中被阻断，而在D-NAME中不被阻断。(4)We提示脑池内注射L-Glu可能通过NMDA受体介导一氧化氮的增加，对神经源性肺水肿的发生具有抑制作用。3.研究了神经肽Y（neuropeptide Y，NPY）对常氧和缺氧状态下大鼠主动脉内皮细胞（RAEC）单层通透性变化的影响。（1）在缺氧状态下，NPY呈剂量依赖性地增加RAEC单层的通透性，而常氧状态下则无此变化。(2)We提示在缺氧状态下，NPY通过NPY-Y3受体增加RAEC单层的通透性。

1.We have evaluated effects of 2 and 4 weeks previous unilateral left-vagotomy on incidence of fibrin induced pulmonary edema and expression of nitric oxide synthase in medulla oblongata in rats. (1)We propose that an increase in nitric oxide, possibly in the nucleus tractus solitarius 2 weeks after left vagotomy, may have an inhibitory action on the development of neurogenic pulmonary edema. (2)Such changes do not occur 4 weeks after left vagotomy.2.By intracisternal injection of L-glutamete (L-Glu) which promote NO release from nerve terminal through NMDA receptor, we evaluated a, role of NO in central nervous system in a neurogenic pulmonary edema. (1)Expression of NMDAR1 is found in only homonymous nucleus tractus solitarii 2 weeks after left vagotomy, and a quantity of NO increases proportionally to the amount of L-Glu. (2)Intracisternal injection of L-Glu decreases incidence of fibrin induced pulmonary edema and amount of pulmonary wet weight. (3)Such inhibitory effect of L-Glu was blocked in L-NAME and MK0-801,but it was not blocked in D-NAME. (4)We propose that an increase in nitric oxide, possibly mediated by intracisternal administration of L-Glu through NMDA receptor, may have an inhibitory action on the development of neurogenic pulmonary edema.3.We have evaluated effects of neuropeptide Y (NPY) on permeability changes in rat aorta endothelial cell (RAEC) monolayer in a state of normoxia and hypoxia. (1)NPY increases permeability of RAEC monolayer in dose dependent manner in a hypoxia state, and these changes were not seen in normoxia. (2)We propose that NPY increases permeability on RAEC monolayer through NPY-Y3 receptor in a hypoxia state.