抄録
We examined the effects of a potent cholecystokinin (CCK) receptor antagonist, L-364, 718 and those of a trypsin inhibitor, camostat mesilate (camostat) after induction of acute pancreatitis with caerulein. Seven intraperitoneal caerulein injections (15μg/kg) were repeated in rats at hourly intervals. The rats were then divided into four treatment groups: oral administration of water plus intraperitoneal injection of a vehicle, polyethylene glycol and glycerin (PEG) ; oral administration of water plus intraperitoneal injection of L-364, 718 in PEG at a dose of 2mg/kg; oral administration of camostat 400 mg/kg a day plus intraperitoneal injection of PEG, and oral administration of camostat plus intraperitoneal injection of L-364, 718. Camostat or water alone was administered once a day beginning 1 h after the last caerulein injection. L-364, 718 or PEG alone was injected every 6h beginning 18h after the last caerulein injection. All observations were made on day 4. The rate of DNA synthesis was determined to evaluate pancreatic regeneration. L-364, 718 inhibited regeneration whether or not camostat was given, while camostat given alone increased plasma CCK, promoted pancreatic DNA synthesis, and decreased the histologic severity of the pancreatitis. Histologic damage in the pancreas was milder in rats receiving both camostat and L-364, 718 compared to those receiving only L-364, 718. Therefore, we conclude that CCK participates in the regeneration of acinar cells after acute pancreatitis in rats, together with other factors.
