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

神经源性肺水肿中枢神经系统病理生理学研究（迷走神经和一氧化氮的作用）

基本信息

批准号：
13671571
负责人：
NISHIWAKI Kimitoshi
金额：
$ 0.77万
依托单位：
Nagoya University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2003
项目状态：
已结题

项目摘要

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.

1.我们评估了2周和4周前单侧左侧迷走神经切断术对大鼠纤维蛋白诱导的肺水肿发生率和延髓一氧化氮合酶表达的影响。 (1)我们认为，左侧迷走神经切断术后 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)左侧迷走神经切断术后4周不会出现这种变化。2.通过脑池内注射L-谷氨酸(L-Glu)，通过NMDA受体促进神经末梢释放NO，我们评估了NO在中枢神经系统中在神经源性肺水肿中的作用。 (1)左侧迷走神经切断术后2周，仅在同名孤束核中发现NMDAR1的表达，并且NO的量与L-Glu的量成比例地增加。 (2)脑池内注射L-Glu可降低纤维蛋白引起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MK0-801中被阻断,但在D-NAME中没有被阻断。 (4)我们提出，一氧化氮的增加可能是通过NMDA受体脑池内给予L-Glu介导的，可能对神经源性肺水肿的发展具有抑制作用。 3.我们评估了神经肽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)NPY在缺氧状态下以剂量依赖性方式增加RAEC单层的通透性，而在常氧状态下没有观察到这些变化。 (2)我们提出NPY在缺氧状态下通过NPY-Y3受体增加RAEC单层的通透性。