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A single dose of the synthetic proteinase inhibitor, Camostat (FOY-305; 100 mg/kg), was administered orally to rats. Pancreata were isolated and then perfused to examine the change in the level of resting fluid secretion. As early as 6 h after administration of the single dose of Camostat, the resting fluid secretion was significantly elevated. Twelve hours after administration, resting fluid secretion was maximally elevated, whereas contents of trypsinogen, chymotrypsinogen, and amylase per DNA in the pancreas were significantly decreased. After 12 h, the level of resting fluid secretion gradually decreased to the control resting level in contrast to significant increases in contents of the pancreatic enzyme and zymogens, and wet weight in acinar cells. We further examined the mechanism mediating the elevated resting fluid secretion. Our results are compatible with the view that the elevation of resting fluid secretion may be maintained by spontaneous activation of ion transporters: an ouabain-sensitive Na-K ATPase, an amiloride-sensitive Na-H antiporter, and a unique Cl transporter that is insensitive to furosemide, bumetanide, SITS, and DNDS. [ABSTRACT FROM AUTHOR]

This study was conducted to elucidate the possible influence of long-term peroral administration of alcohol on the repair process of acute necrotizing pancreatitis. Male Wistar rats fed with balanced diet were divided into two groups. The first group had free access to 15% ethanol, and the second group, the control group, has access to water instead. After fifty weeks, acute necrotizing pancreatitis was induced in rats by infusing 0.4% lysolecithin into their pancreatic duct. In the course of pancreatitis, pancreatic enzymes in serum, enzymes and protein in pancreas, and DNA synthesis in pancreas in both groups, changed in the same way. Histologically, interstitial edema, necrosis of parenchyma, infiltration of inflammatory cells, and formation of tubular complex were observed. Most of these histological changes of pancreas in both groups disappeared in twenty days and pancreas was repaired almost completely. These findings suggest that the repair process of acute necrotizig pancreatitis is not affected by preceding long-term intake of alcohol. [ABSTRACT FROM AUTHOR]