| 1. |
- Friman, Styrbjörn, 1948, et al.
(författare)
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Hepatobiliary compensation for the loss of gallbladder function after cholecystectomy. An experimental study in the cat.
- 1990
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Ingår i: Scandinavian journal of gastroenterology. - 0036-5521. ; 25:3, s. 307-14
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Tidskriftsartikel (refereegranskat)abstract
- The side effects of the removal of a functioning gallbladder are surprisingly few, and it has been suggested, but never demonstrated, that the hepatobiliary tract then adjusts to compensate for the loss of gallbladder function. In this study the effects of cholecystectomy on bile acid kinetics, bile flow, and biliary clearance of mannitol were studied in cats 6-8 weeks after cholecystectomy. An enhanced recycling rate of a diminished bile acid pool was found. The bile flow was reduced and the bile acid concentration in hepatic bile was increased, but fasting bile acid secretion rate was not changed. Both when the bile acid secretion rate was reduced by drainage via an acute bile fistula and when it was enhanced by intravenous infusion of glycocholic acid, there was a lower bile acid-independent flow in the cholecystectomy group. This reduced bile flow after cholecystectomy was not explained by the higher proportion of deoxycholic acid present in the bile of the cholecystectomized animals. Biliary clearance of mannitol, which is supposed to reflect the canalicular inflow, was not reduced, indicating that the reduction in bile flow is explained by a reduced fluid secretion or an enhanced fluid reabsorption in the bile ductules and ducts after cholecystectomy. In this manner the bile ducts compensate for the loss of the absorptive function of the gallbladder after cholecystectomy.
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| 2. |
- Nilsson, Bengt E, 1949, et al.
(författare)
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In vivo regulation of mucosal transport of H+ and HCO3- in the feline gall bladder.
- 1993
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Ingår i: Acta physiologica Scandinavica. - 0001-6772. ; 148:4, s. 403-11
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Tidskriftsartikel (refereegranskat)abstract
- In the gall bladder of a fasting subject, a decline in the pH of the contents occurs due to secretion of H+ from the mucosa. In this study in anaesthetized cats, the gall bladder lumen was perfused with a bicarbonate buffer bubbled with 4% CO2 in air. During basal conditions, the PCO2 always rose while the pH and [HCO3-] fell in the buffer when passing through the gall bladder lumen, indicating a continuous secretion of H+ by the mucosa. This H+ secretion was enhanced by stimulation of the respective sympathetic nerves and was blocked by intraluminal amiloride. Intravenous infusion of vasoactive intestinal peptide (VIP) raised the pH and [HCO3-] in the buffer during the passage through the gall bladder lumen, indicating a secretion of bicarbonate from the mucosa. In view of the presence of sympathetic and VIP immunoreactive nerve fibres in the gall bladder wall and VIP receptors on the luminal epithelial cells, the study demonstrates that there are functional grounds for physiological variations in the secretion of H+ and HCO3- by the gall bladder mucosa. These variations may be important for the solubility of calcium salts in the gall bladder contents.
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