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Neurogenic Inflammation of Guinea‐Pig Bladder
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Capsaicin, substance P, and ovalbumin, instilled into the bladders
of naive and ovalbumin (OVA) sensitized guineapigs caused
inflammation, as indicated by increased vascular permeability.
Histological changes after exposure to these compounds progressed
with time from intense vasodilatation to marginalization of
granulocytes followed by interstitial migration of leukocytes. In
vitro incubation of guinea‐pig bladder tissue with substance P and
ovalbumin stimulated release of prostaglandin D2 and leukotrienes. In
vitro incubation of bladder tissue with capsaicin, OVA,
prostaglandin D2, leukotriene C4, histamine, or calcium ionophore
A‐23587 all stimulated substance P release. These data suggest that
bladder inflammation initiated by a variety of stimuli could lead to
a cyclic pattern of release of inflammatory mediators and
neuropeptides, which could result in amplification and persistence
of cystitis after the inciting cause has subsided.
Title: Neurogenic Inflammation of Guinea‐Pig Bladder
Description:
Capsaicin, substance P, and ovalbumin, instilled into the bladders
of naive and ovalbumin (OVA) sensitized guineapigs caused
inflammation, as indicated by increased vascular permeability.
Histological changes after exposure to these compounds progressed
with time from intense vasodilatation to marginalization of
granulocytes followed by interstitial migration of leukocytes.
In
vitro incubation of guinea‐pig bladder tissue with substance P and
ovalbumin stimulated release of prostaglandin D2 and leukotrienes.
In
vitro incubation of bladder tissue with capsaicin, OVA,
prostaglandin D2, leukotriene C4, histamine, or calcium ionophore
A‐23587 all stimulated substance P release.
These data suggest that
bladder inflammation initiated by a variety of stimuli could lead to
a cyclic pattern of release of inflammatory mediators and
neuropeptides, which could result in amplification and persistence
of cystitis after the inciting cause has subsided.
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