Neurogenic inflammation in the nasal mucosa is caused by neuropeptides such as substance p, released from sensory nerve endings. The effects of substance P are decreased by neutral endopeptidase(NEP), which is a peptidase that degrades substance
P
and
other sensory neuropeptides.
In this present study, we used capsaicin(100%㎍/㎏ iv) to produce neurogenic inflammation in the septal mucosa of rats, and we examined the effect of phosphoramidon(2.5㎎/㎏iv ) on neurogenic inflammation(vascular permeability). Sites of
increased
vascular permeability were localized with Monastral blue. In rats that received Monastral blue alone, no extravasated blood vessels were found in the septal mucosa, whereas capsaicin or phosphoramidon alone caused only slight extravasation of
Monastral
blue pigment in the anterior septal mucosa(3.04±0.81㎜/0.2㎟). When the phosphoramidon was followed by the capsaicin, many venules were labelled with Monastral blue(7.22±1.89㎜/0.2㎟). On the other hand, when the vehicle was preceded by
phosphoramidone, an few venules were labelled in the anterior septal mucosa(1.29㎜/0.2㎟).
We conclude that decreased NEP activity may cause the increased susceptibility to neurogenic inflammation by allowing higher concentration of substance p to reach tachykinin receptor in the nasal mucosa. Thus decreased NEP activity may exacerbate
some
of the pathologic response in the nasal mucosa. (Korean J Otolaryngol 39 : 3, 1996)
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