A. Dembinski et al., INFLUENCE OF CAPSAICIN-SENSITIVE AFFERENT NEURONS AND NITRIC-OXIDE (NO) ON CERULEIN-INDUCED PANCREATITIS IN RATS, International journal of pancreatology, 19(3), 1996, pp. 179-189
Conclusion. Stimulation of afferent neurons by capsaicin exerts protec
tive activity against cerulein-induced pancreatitis, This action is de
pendent on endogenous release of nitric oxide (NO), Deactivation of af
ferent neurons by high doses of capsaicin contributes to the severity
of pancreatitis, This action involves mainly decreased pancreatic bloo
d flow (PBF), Afferent nerves and NO cooperate in the maintenance of t
he integrity of pancreatic tissue. Background. Stimulation of capsaici
n-sensitive afferent fibers protects gastric mucosa against damage and
causes changes in mucosal blood flow. The aim of the present study wa
s to determine the role of stimulation or ablation of capsaicin-sensit
ive neurons and NO in the course of cerulein-induced pancreatitis in t
he rat. Methods. Low and high doses of capsaicin were administered to
animals with pancreatitis and to those without pancreatitis. The effec
t on several parameters was assessed. NO activity was blocked by N-G-n
itro-L-arginine. Results. We found that a low dose of capsaicin admini
stered intragastrically caused an increase in PBF. A neurotoxic dose o
f capsaicin caused a decrease in PBF, RNA content, and DNA synthesis.
Pancreatitis led to a significant decrease in PBF and DNA synthesis, b
ut an increase in pancreatic weight, protein content, plasma amylase c
oncentration, and neutrophil adherence. Stimulatory doses of capsaicin
attenuated the pancreatic tissue damage of pancreatitis, and alterati
on of PBF, DNA synthesis, and neutrophil adherence. Capsaicin-induced
ablation of afferent neurons caused an increase in all indicators of p
ancreatic damage. Blocking NO enhanced pancreatic damage, and this was
reversed by addition of L-arginine.