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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    World journal of surgery 3 (1979), S. 449-456 
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé La formation de bile dépend principalement de l'excrétion des sels biliaires par le foie; celle-ci est contrôlée par la circulation entéro-hépatique qui ramène les sels biliaires au foie, et par la synthèse de nouveaux sels biliaires. Plusieurs hormones gastro-intestinales, la sécrétine, la CCK, la gastrine sulfatée et le glucagon, augmentent le volume de la sécrétion biliaire et l'excrétion biliaire d'électrolytes; mais aucune d'entre elles n'influence la sécrétion de sels biliaires. L'action de la sécrétine est physiologique. La gastrine non sulfatée et la pentagastrine ne sont pas cholérétiques. L'effet cholérétique des dérivés de la CCK dépend de la présence de tyrosine sulfatée en position 7. Les catécholamines augmentent le débit biliaire par un mécanisme qui fait intervenir les récepteurs bêta, mais dont les détails sont encore inconnus. Le rôle du système nerveux parasympathique est mal précisé. Rien ne prouve que la sécrétion hépatique de sels biliaires soit sous contrôle nerveux. Le tonus de la vésicule biliaire et du sphincter d'Oddi contrôle la quantité de bile qui entre dans le duodénum. La CCK est la seule hormone gastro-intestinale dont l'activité cholécystocinétique soit démontrée. Elle provoque la contraction de la vésicule et l'ouverture du sphincter d'Oddi par une action directe sur ces organes. Le système nerveux parasympathique joue probablement un rôle dans la régulation du tonus musculaire de la vésicule.
    Notes: Abstract The primary determinant of bile formation is the hepatic excretory rate of bile salts, which is controlled by the rate of return of bile salts to the liver by the enterohepatic circulation and by the synthesis of new bile salts. The gastrointestinal hormones secretin, cholecystokinin (CCK), sulfated gastrin, and glucagon increase bile volume and inorganic ion excretion into bile, but none of them influence bile salt secretion. The action of secretin is clearly physiologic. Nonsulfated gastrin and pentagastrin are not choleretics. The choleretic property of CCK derivatives is dependent upon the presence of sulfated tyrosine at position 7. Catecholamines increase bile flow by a mechanism that involves beta receptors, but the precise mechanism is unknown. The role of the parasympathetic nervous system is not clear. There is no evidence that hepatic secretion of bile salts is under neural control. The tone of the gallbladder and sphincter of Oddi regulates the amount of bile that actually enters the duodenum. CCK is the only known physiologic cholecystokinetic gastrointestinal hormone. It contracts the gallbladder and relaxes the sphincter of Oddi by direct action on the muscle of these structures. The parasympathetic nervous system probably participates in regulation of gallbladder muscle tone.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Ion transport and electrical properties of rabbit and guinea pig gallbladders were investigated to gain further information about the active transport mechanism that mediates fluid absorption. The intracellular and transepithelial electrical potentials were measured simultaneously using the microelectrode technique. Exposure of the mucosal surface to Amphotericin B resulted in the prompt development of a serosa-positive electrical potential difference (PD) which could not be attributed to an alteration in ion diffusion potentials across either the cell membrane or across the tight junction. Because the Amphotericin B-inducedPD was immediately dependent on warm temperatures and O2, and was independent of NA and K concentration gradients across the cell membrane, it is suggested that active ion transport is directly responsible for thePD. Since thePD was abolished in the absence of Na in the bathing solutions, a rheogenic Na pump is postulated; this pump also appears to be operative in tissue not exposed to Amphotericin B. The specific tissue properties altered by Amphotericin B to produce a serosa-positivePD remain incompletely defined. The results of the present study indicate that ion transport by rabbit gallbladderin vitro is a consequence of a rheogenic active Na transport mechanism at the basolateral membranes which, in conjunction with a coupled NaCl influx process at the mucosal border, ultimately results in absorption of NaCl and water.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    The journal of membrane biology 37 (1977), S. 277-297 
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Previous studies have led to the suggestion that salt and water absorption by rabbit and guinea pig gallbladders exposed to Amphotericin B proceeds by a rheogenic Na pump at the basolateral cell membrane. The present studyin vitro was designed to further characterize transport properties of rabbit and guinea pig gallbladders under control conditions and to identify the properties of gallbladder mucosa which are altered by Amphotericin B to allow for the induced serosa-positive electrical potential differences (PD). Potassium is required in the bathing solution at a low concentration to maintain normal tissue O2 consumption, fluid absorption and the ability of the tissue to develop the maximum Amphotericin B-induced PD; the relative effectiveness of alkali metal cations in substituting for K is K≥Rb〉Cs〉Li〉Na. The carrier mechanism for coupled influx of Na and Cl across the mucosal border of gallbladder appears to be functional in the presence of Amphotericin B; in addition, the diffusional influx of chloride is not significantly altered by the antibiotic. The primary action of Amphotericin B which appears to modify rabbit and guinea pig gallbladders from having transmural PD's of less than ±1 mV to having serosa-positive PD's of 5–30 mV is an increase in the mucosal cell membrane permeability to Na. This permeability change has the effect of partially uncoupling NaCl influx. A rheogenic Na pump mechanism at the basolateral membrane, presumably in operation under control conditions also, may account for the PD.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    World journal of surgery 13 (1989), S. 320-320 
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    World journal of surgery 15 (1991), S. 626-627 
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    World journal of surgery 2 (1978), S. 618-619 
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Abdominal imaging 17 (1992), S. 283-284 
    ISSN: 1432-0509
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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