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Gastrin has been proposed as a trophic factor for the pancreas. Extensive small-bowel resection increased transiently plasma gastrin levels in the rat and produced pancreatic growth. This growth was characterized by an increased pancreatic weight, protein and DNA content, and the occurrence of mitotic figures in acinar cells. In order to determine if gastrin is implicated in pancreatic hyperplasia, we induced endogenous variations of gastrin 3 weeks before small-bowel resection or transection. Hypogastrinemia was produced by antrectomy and hypergastrinemia by vagotomy plus pyloroplasty. Pyloroplasty alone was without any effect. All gastric operations alone enhanced though not significantly the weight of the pancreas and its content in protein and DNA. When performed before intestinal resection, they did not modify the hyperplastic response of the pancreas to the resection. Our findings do not support the views that antral gastrin exerts a trophic action on the rat pancreas and that gastrin is implicated in postresectional hyperplasia of the gland.

To determine whether intestinal bypass operation and alcohol administration exerted a synergistic effect on pancreatic enzyme composition and morphology, adult rats were submitted either to a sham-operation or to a 90 per cent jejunoileal bypass. Two weeks after the operation, the rats received a 15 per cent solution of ethanol in drinking fluid during a period of four weeks while controls received water. In sham-operated animals, alcohol had no effect on pancreatic weight or its total content in protein and amylase. The general structural and ultrastructural aspect remained unchanged except for the presence of a few mixed acinar-islet cells. Bypass operation alone induced a significant decrease in amylase content while the population of zymogen granules was reduced. Parallely, lipid droplets deposited within acinar cells. Alcohol administered in bypassed animals exerted a synergistic effect on fat accumulation in pancreatic acinar cells but had no effect on other biochemical and morphological parameters.

The rare instance of a gastrointestinal hemorrhage caused by a lithiasis of the duct of Wirsung is described. The world literature records only 13 other cases. Pancreatic calculi cause hemorrhage by either migrating through the pancreatic parenchyma to perforate the duodenum, ulcerating the vessels of the periductal parenchyma, or rupturing the pancreas. The usual sign of this complication of chronic calcifying pancreatitis, difficult to diagnose, is repeated gastrointestinal hemorrhages and sometimes pain, as in epigastric colitis. The immediate therapy is control of the hemorrhage. With transcatheter occlusive techniques, radical surgery can be postponed until it is more tolerable.

Bombesin administered subcutaneously to rats, three times daily for four days, induces pancreatic growth at a dose of 10 micrograms/kg. Growth was characterised by an increased pancreatic weight and content in protein and RNA, accompanied by cellular hypertrophy. Chronic bombesin also enhanced the pancreatic content in chymotrypsin and to a lesser degree its contents in amylase and lipase. The volume of the secretion and the output of enzymes in response to CCK under an infusion of secretin, however, remained unchanged although the functional capacity of individual cells to secret amylase and lipase was reduced. It is concluded that chronic bombesin exerts a trophic action on the rat pancreas but decreases the sensitivity of each cell to hormonal stimulation.

This work investigates the effect, on the rat pancreas, of a chronic administration of bombesin in function of the dose and duration of treatment and examines whether this effect may be mediated by the release of endogenous gastrin or cholecystokinin. Bombesin, administered three times daily for 5 or 15 days, induced a marked increase in pancreatic weight, its protein, RNA and enzyme contents with the dose of 10 micrograms/kg body weight; the ratios of pancreatic weight, protein and RNA contents to DNA contents increased significantly after a 5 day treatment, suggesting cellular hypertrophy. Pancreatic DNA content was markedly enhanced after a 15 day treatment, suggesting cellular hyperplasia. Antrectomy decreased plasma gastrin levels, but did not alter the pancreatico-trophic action of a 10 micrograms/kg bombesin treatment for 5 days. Proglumide, an inhibitor of cholecystokinin and gastrin in the pancreas, did not affect the growth of the pancreas induced by a 10 micrograms/kg bombesin treatment for 5 days. It is concluded that chronic bombesin induces, in the rat pancreas, cellular hypertrophy or hyperplasia depending on the duration of treatment. Pancreatic hypertrophy is not mediated by the release of endogenous gastrin or cholecystokinin.

To determine whether jejunoileal bypass operation and alcohol administration exerted a synergistic effect on the activities of brush border membrane enzymes and on liver morphology, adult rats where submitted either to sham operation or to jejunoileal bypass operation. 2 weeks after operation the rats received a 15% solution of ethanol during a period of 4 weeks, controls received water. In the sham-operated rats, alcohol provoked stimulation of the disaccharidase activities in the proximal jejunum but had no effect on these activities in the ileum. Bypass operation alone induced a significant increase in sucrase activity in the functioning ileum but had no effect on the jejunal disaccharidase activities. Alcohol administered after bypass provoked a further increase in ileal brush border sucrase activity. The increase of the brush border enzyme specific activities in the excluded loop resulted from the important protein loss observed in this segment. Alcohol alone or bypass operation by itself had little effect on liver morphology. In contrast, when associated they induced extensive accumulation of fat droplets in the hepatocytes. Since alcohol is frequently associated with the diet in man, alcohol should be considered as an important contributing factor to intestinal enzyme adaptation and liver dysfunction after jejunoileal bypass operation.

This work investigates the pancreatico-trophic action of bombesin, a peptide stimulating pancreatic secretion in vivo and in vitro and examines whether this effect is altered by CCK or secretin. Rats were injected three times daily for 5 days either with saline, bombesin (1 or 10 micrograms/kg), CCK (20 I.D.U./kg), secretin (20 C.U./kg) or a combination of bombesin and CCK or secretin. Bombesin alone induced growth of the pancreas beginning with the dose of 10 micrograms/kg. This growth was characterized by an increase of pancreatic weight, its protein, RNA and enzyme content, but not of its DNA content. The ratios of the three former parameters to DNA increased, suggesting cellular hypertrophy. Cholecystokinin alone exhibited a similar trophic action on the pancreas as bombesin. Secretin alone had no effect on pancreatic size and composition. Cholecystokinin and secretin did not modify the pancreatico-trophic response of bombesin. These findings suggest that bombesin, administered for 5 days in the rat, induces pancreatic growth due to cellular hypertrophy. Cholecystokinin has the same effect. However the mode of action, at the cellular level, of bombesin appears to be different from that of cholecystokinin.