| Summary: | 碩士 === 國立中山大學 === 生命科學研究所 === 83 === Acute inflammation caused by stimulating sensory nerves is
called 〝neurogenic inflammation〞. Neurogenic inflammation
occurs when the supplying sensory axons are stimulated by
irritant substances. The syndromes of neurogenic inflammation
in airways include increased vascular permeability,
degranulation of goblet cells。 The vagal sensory axon release
substance P which can exerts the permeability－increasing
effect on the venular endothelium and mucus－discharging effect
on the goblet cells. Sensory nerves can be destroyed by
treating the neonates with high dose of capsaicin（50 mg/kg）.
In this present study we sought to know if neonatal capsaicin
could affect the neurogenic plasma extravasation and the mucous
secretion of goblet cells in the adults. Capsaicin（90 ug/kg）
or substance P（3 ug/kg）was injected to test the permeability
of venules and mucus－secreting ability in the airways of adult
rats that had neonatally been pretreated with capsaicin. Indian
ink was used to label the leaky venules and to measure their
area density in the whole mounts. To investigate cell and
tissue responses of the mucosa, histological methods were
employed. The area density of Indian ink－labeled venules
decreased by 69﹪. Extravasation by substance P did not
decrease. These findings suggest that neonatal capsaicin could
not inhibit the development of microvasculature and the number
of venules did not decrease. Histological study indicated that
the development of mucosal surface epithelium in trachea of
adult rats, after neonatal capsaicin treatment was changed.
There was only a few goblet cells. The number of ciliated cell
was reduced. These observations suggest that mucus－secreting
function was impaired in the airways in rats neonatally treated
with capsaicin.
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