Influence of biliary diversion upon gastric acid secretion.

Sekine, Takeshi; Tsukui, Hajime; Kameyama, J; Sasaki, Iwao; Sato, Toshio

doi:10.1620/tjem.134.125

Cited by 4 publications

(1 citation statement)

References 11 publications

(15 reference statements)

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“…The duodenal acidification we observed in pigs with no bile restitution might be a result of excess gastric acid secretion, as shown by Sekine et al (1981b) (Malagelada, 1980 (Laplace, 1978) (Corring, 1980), it is necessary to define the quantity of enzymes rendered inactive by acid compared to the total amount excreted into the duodenum.…”

Section: Introductionmentioning

confidence: 99%

Contribution of bile and pancreatic juice to the control of pH in the pig duodenum

Abello¹,

Corring²,

Laplace³

et al. 1987

Reprod. Nutr. Dévelop.

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Summary. To evaluate the respective contributions of biliary and pancreatic secretions in the formation of intraduodenal pH, 10 pigs were chronically fistulated in either the common bile duct (5 pigs) or the pancreatic duct (5 pigs). They were all fitted with a permanent catheter into the duodenum for the continuous return of secretion and with a duodenal Tcannula allowing the introduction of a combined glass electrode. pH was recorded over 8-hour periods in fed or fasted pigs in which both secretions were returned or in which either the bile or the pancreatic juice was not restituted. In fed pigs with secretions normally flowing into the duodenum, the pH fluctuated between 4 and 6 during 57 % of the recording time ; it exceeded 6 during 29 % of this period. The rest of the time, it remained between 2 and 4. Bile deprivation did not change the duration of the 4 < pH < 6 and 2 < pH < 4 ranges, although a slight decrease of the pH > 6 time-course was recorded.Deprivation of pancreatic secretion did not induce significant variations of the pH pattern.In fasted pigs with restituted biliary and pancreatic secretions, a pH > 6 was recorded for 70 % of the 8-hour period. The pH was lower in short periods : 19 % (4 < pH < 6), 8 % (2 < pH < 4) and less than 1 % (pH < 2) of the time. Total suppression of bile as well as that of pancreatic juice resulted in a significant decrease of the pH > 6 range to the benefit of the acid periods which were increased. These observations suggest that, in fed pigs, food temporarily surpassed the neutralizing abilities of the digestive secretions, but that, in fasted pigs, biliary and pancreatic secretions were important in the neutralization of duodenal juice.Introduction.

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Section: Introductionmentioning

confidence: 99%

Contribution of bile and pancreatic juice to the control of pH in the pig duodenum

Abello¹,

Corring²,

Laplace³

et al. 1987

Reprod. Nutr. Dévelop.

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Biliary and pancreatic secretions influence experimental duodenal ulcer without affecting gastric secretion in the rat

1985

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The effect of the absence of biliary and/or pancreatic secretions in the duodenum or the enhanced presence of bile at the proximal duodenum on the incidence, severity, number, and location of cysteamine-induced duodenal ulcers was investigated in the rat. Cysteamine produced ulcers on the anterior wall of the duodenum in 75% and on the posterior wall ("kissing ulcers") in 50% of the animals. Diversion of biliary and/or pancreatic secretions from the duodenum increased both the severity and the incidence of the posterior duodenal ulcers. Diversion of bile to the proximal duodenum, on the other hand, decreased the severity as well as the incidence of the anterior duodenal ulcers. Mortality in rats receiving cysteamine correlated with the severity of ulcers. Taurocholic acid at nontoxic doses given subcutaneously or orally to nonoperated rats and rats which had bile diverted to the proximal duodenum aggravated the cysteamine-caused duodenal ulcers. Neither proximal nor distal diversion of bile had a major effect on gastric secretion of acid and pepsin in normal or cysteamine-treated rats. We conclude that both bile and pancreatic secretions may directly influence the development of cysteamine-induced duodenal ulcers in the rat.

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