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

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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.