Effect of Selective and Truncal Vagotomy on Insulin-Stimulated Bile Secretion in Dogs

Geist, Richard E.; Jones, R. Scott

doi:10.1016/s0016-5085(71)80061-6

Cited by 24 publications

(5 citation statements)

References 14 publications

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“…Insulin increases inorganic ion output in bile, probably by stimulation of the bile salt-independent fraction of canalicular secretion, but has no effect on bile salt output. Insulin choleresis is not completely blocked by vagotomy, suggesting that its effect is not mediated by the vagi [13,14]. We found that atropine blocks insulin choleresis in dogs [16], but this finding has not been confirmed by others [15].…”

Section: Neural Control Of Hepatic Bile Formationcontrasting

confidence: 64%

“…Insulin choleresis is not completely blocked by vagotomy, suggesting that its effect is not mediated by the vagi [13,14]. We found that atropine blocks insulin choleresis in dogs [16], but this finding has not been confirmed by others [15]. It is possible that insulin stimulates bile flow by a cholinergic mechanism that is not mediated by the vagus nerves.…”

Section: Neural Control Of Hepatic Bile Formationcontrasting

confidence: 54%

“…Direct electrical stimulation of the vagus nerves in dogs had no effect on bile flow when the enterohepatic circulation was intact and gastric secretions, which increased by the technique used, were prevented from entering the duodenum, where they could cause secretin release [12]. There is good evidence in dogs that vagotomy does not alter basal bile flow over a wide range of bile salt excretion rates [13,14]. Atropine, used as a vagal blocker, has no effect on bile flow at low rates of bile salt excretion [15], but increases bile flow at high rates of bile salt excretion [16].…”

Section: Neural Control Of Hepatic Bile Formationmentioning

confidence: 99%

“…There is good evidence in dogs that vagotomy does not alter basal bile flow over a wide range of bile salt excretion rates [13,14]. Atropine, used as a vagal blocker, has no effect on bile flow at low rates of bile salt excretion [15], but increases bile flow at high rates of bile salt excretion [16]. Atropine produces a choleresis in the perfused cat liver, which suggests that the effect may not be vagally mediated [17].…”

Section: Neural Control Of Hepatic Bile Formationmentioning

confidence: 99%

“…Insulin hypoglycemia, which stimulates parasympathetic activity, is associated with increased hepatic bile flow [13]. Insulin increases inorganic ion output in bile, probably by stimulation of the bile salt-independent fraction of canalicular secretion, but has no effect on bile salt output.…”

Section: Neural Control Of Hepatic Bile Formationmentioning

confidence: 99%

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Neurohormonal control of biliary secretion and gallbladder function

Kaminski

Nahrwold

1979

World J. Surg.

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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.Bile salts, the primary constituents of bile, participate in digestion of fats and the absorption of lipids. Bile also serves as the vehicle for hepatic excretion of bilirubin, phospholipids, cholesterol, and some lipid soluble drugs and metabolites that cannot be eliminated by the kidney.Bile formation begins in bile canaliculi, 0.6-1.2/zm channels that are formed by portions of the

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Section: Neural Control Of Hepatic Bile Formationcontrasting

confidence: 64%

Section: Neural Control Of Hepatic Bile Formationcontrasting

confidence: 54%

Section: Neural Control Of Hepatic Bile Formationmentioning

confidence: 99%

Section: Neural Control Of Hepatic Bile Formationmentioning

confidence: 99%

Section: Neural Control Of Hepatic Bile Formationmentioning

confidence: 99%

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Neurohormonal control of biliary secretion and gallbladder function

Kaminski

Nahrwold

1979

World J. Surg.

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Muscarinic acetylcholine receptor stimulation of biliary epithelial cells and its effect on bile secretion in the isolated perfused liver

et al. 1997

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has been identified as secretagogue. The observed increase The aim was to explore whether biliary epithelial cells in bile flow is of ductular origin. 4,5 Recent findings in biliary show muscarinic acetylcholine receptors and to investiepithelial cells have elucidated the mechanism of secretin gate their role in ductular bile formation. In both, isoinduced choleresis. investigated in a model with a high proportion of ductular bile flow, namely the isolated perfused guinea pig. Biliary epithelial cells line the intra-and extrahepatic biliary tree. They begin with small cuboidal cells at the canal of MATERIALS AND METHODS Hering and form ultimately the extrahepatic common bile Materials.Male Wistar rats (250-300 g) and guinea pigs were duct.1,2 Although biliary epithelial cells account for only 3% obtained from the animal facilities of the University of Heidelberg, to 5% of the overall population of liver cells, this epithelium and housed in temperature and humidity controlled animal quarters provides a large surface area for electrolyte and fluid ex-on a 12-hour light/dark cycle. They were allowed free access to the standard chow and tap water until the time of the study. The animal change.3 Several hormones are involved in intestinal fluid experiments had been reviewed and permitted by a state board on secretion and absorption. In biliary epithelial cells secretin animal experimentation. Collagenase type I, carbamylcholine chloride (carbachol), and 2,5-di-tert-butylhydroquinone (tBuBHQ) were obtained from Sigma (Munich, FRG). DNAse type I, pronase, and trypsin were from Boeh- (1,1-dioctadedyl-3,3,3-tetra methylindocarbocyanine perchlorate) Received August 2, 1996; accepted December 20, 1996. (Dil-Ac-LDL) were from Molecular Probes Inc. (Eugene, OR). All first perfused for 15 minutes with a gazed buffer of 0.2 mmol/L eg-

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Mechanisms of Bile Secretion and Hepatic Transport

Boyer

1986

Physiology of Membrane Disorders

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Effect of Selective and Truncal Vagotomy on Insulin-Stimulated Bile Secretion in Dogs

Cited by 24 publications

References 14 publications

Neurohormonal control of biliary secretion and gallbladder function

Neurohormonal control of biliary secretion and gallbladder function

Muscarinic acetylcholine receptor stimulation of biliary epithelial cells and its effect on bile secretion in the isolated perfused liver

Mechanisms of Bile Secretion and Hepatic Transport

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