Conclusions: Octreotide treatment contributes to the regulation of tumor ne
crosis factor (TNF) production in sodium taurocholate-induced acute necroti
zing pancreatitis in rats. Owing to its complex effect, octreotide can part
ially ameliorate the deleterious consequences of acute necrotizing pancreat
itis. Elevated TNF and interleukin-6 (IL-6) levels in the peritoneal fluid
may be considered a consequence of the activation of peritoneal macrophages
.
Background. The effects of octreotide on exocrine pancreatic function have
been investigated in numerous studies, but little attention has been paid t
o its influence on cytokine production in acute pancreatitis.
Methods. Acute pancreatitis was induced by the retrograde injection of taur
ocholic acid into the pancreatic duct in male Wistar rats. Serum amylase ac
tivity, wet pancreatic weight/body weight (pw/bw) ratio, and TNF and IL-6 l
evels were measured. Four mu g/kg of octreotide was administered subcutaneo
usly at the time of induction of pancreatitis and 24 or 48 h later. Rats we
re sacrificed 6, 24, 48, or 72 h after the operation.
Results. The serum amylase level and pancreatic weight to body weight ratio
were decreased significantly in the octreotide-treated group. The serum TN
F level was decreased significantly in the octreotide-treated group as comp
ared with the control group at 6, 24, and 48 h (0.6 +/- 1.5, 2.0 +/- 3.3, a
nd 0 vs 50 +/- 15.5, 37.5 +/- 18.4, and 13.1 +/- 12.5 U/mL, respectively).
The ascites TNF level was decreased to 0 in the octreotide-treated group an
d was elevated in the control group at 72 h (28.0 +/- 49.0 U/mL). IL-6 prod
uction in ascites was extremely high in both groups at 6 h (80,000 +/- 43,
817 pg/mL and 58, 500 +/- 33 335 pg/mL), but the difference was not signifi
cant.