Lectin-binding studies have been performed on rat zymogen granules to investigate alterations in the
carbohydrate membrane composition that occur in
acute pancreatitis induced by
caerulein. The influence of treatment with
hydrocortisone for seven days before inducing
pancreatitis was also studied.
Lectin labeling on zymogen granules was also analyzed seven days after inducing
pancreatitis in rats that had previously received a
hydrocortisone treatment. During this period
L 364,718 (0.1 mg/kg)--specific
cholecystokinin (
CCK) receptor antagonist--was administered daily to some of the rats, and no treatment was applied to others. Using
fluorescein-labelled T. purpureus (TP)
lectin, a significant decrease in the amount of L-
fucose in the granule membrane was observed in rats with
caerulein-induced
pancreatitis. This effect was directly caused by the
pancreatitis and was not influenced by previous
hydrocortisone treatment. Seven days later, the density of
TP receptors in the granule membrane was similar to the controls both in L-364,718-treated and untreated rats. Therefore, we suggest that endogenous CCK is not an essential factor in the recovery of L-
fucose containing
glycoconjugates the granule membrane after
pancreatitis.
Acute pancreatitis did not alter the expression of
wheat germ agglutinin (WGA) receptors in the zymogen granule membrane. WGA specifically binds
N-acetyl glucosamine and
sialic acids.
L 364,718 administered for seven days after inducing
pancreatitis significantly reduced WGA binding, untreated rats showed a normal zymogen granule membrane. Therefore, the blockade of CCK-induced alterations in membrane
glycoconjugates enriched in
N-acetyl glucosamine and
sialic acid of newly formed granules after
pancreatitis, a finding that could explain the delay in the regression of the disease.