Vagal and spinal sensory afferent innervation are responsible for to regulation of neurogenic inflammation in the airways. Neurogenic inflammation is a complex process involving vasodilatation,plasma protein extravasation and edema,glandular secretion and immunoinflammatory cell chemotaxis and activation. Plasma extravasation is the result of the activation of sensory nerve endings and the subsequent prodution of neuropeptides, namely, tachykinins such as substance P, neurokinin A and neurokinin B. SP was more potent than NKA or NKB in increasing microvascular permeability, which indicate that tachykinin NK-1 receptors are mainly involved in neurogenic inflammation in the airways of rat. When 6-hydroxydopamine¡]6-OHDA¡^was infused into the tracheal lumen,it causes plasma extravasation in the tracheal mucosa mediated by sensory nerve axons. Local application of 6-OHDA to stellate ganglion, had no effect on neurogenic inflammation and SP-IR innervation in the airways.The present study was to investigate the effect of intravenous injection of 6-OHDA on plasma leakage in the airways.This study also used the NK-1 receptor antagonist L-732,138 to investigate if 6-OHDA-induced plasma leakage in the airways was related to NK-1 receptors. India ink was used as tracer dye to label the leaky microvessels to evaluate the magnitude of inflammation . We found that 6-OHDA in the doses of 25 mg/kg and 50 mg/kg caused an extensive increase in plasma extravasation in the trachea and bronchi. But the vehicle¡]1 ¢ML-ascorbic acid and 0.4 ¢MNaCl, pH 3.4¡^caused a slight plasma leakage. Intravenous administration of L-732,138 decrease 6-OHDA induced plasma leakage. But one week after vagal transection, 6-OHDA-induced plasma extravasation in the ipsilateral airways was not significatly reduced. It is suggested that intravenous 6-OHDA stimulated bronchopulmonary C-fibers and resulted in vagal C-fiber release of tachykinins that produced acute inflammation in the lower airways. Intravenous application of L-732,138 significantly reduced the 6-OHDA-induced plasma leakage, suggesting that NK-1 receptors in the venular endothelial cells mediate the inflammatory response in the layynx,trachea,bronchi.and esophagus of the rat .

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