Effect of electrical vagal stimulation on canine hepatic bile flow

Dl, Kaminski; Dorighi, John A.; Jellinek, Max

doi:10.1152/ajplegacy.1974.227.2.487

Cited by 40 publications

(18 citation statements)

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“…Kaminski et al [14] find the role of the posterior vagus most important and that of the anterior vagus practically inexistent. As mentioned before, this view is countered by Daniel and Sarna [6] who found a majority of posterior trunks not even reaching the antrum.…”

Section: Discussionmentioning

confidence: 97%

“…Firstly, the exocrine re sponse of the pancreas to vagal stimulation in the dog may be insufficient. Indeed, in each species the number of ganglia present in the pancreas is different [14]. In the dog pan creas the small number of ganglia correlates well with the failure to elicit stimulation of exocrine secretion [4], Secondly, no signifi cant change in pancreatic enzyme secretion may be found due to the neutralization of a decrease in volume by an increase in enzyme activity in the juice.…”

Section: Discussionmentioning

confidence: 99%

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Pancreatic Function after Seromyotomy of the Canine Stomach

Hee¹,

Verhulst²,

Schil³

1988

Eur Surg Res

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Anterior gastric seromyotomy combined with posterior truncal vagotomy has been proposed as an acid-reducing operation for patients with duodenal ulcer. Section of the posterior vagal trunk could, however, be held responsible for reduced pancreatic function, seen in patients after bilateral truncal vagotomy. In this study the pancreatic function after anterior gastric seromyotomy and posterior truncal vagotomy has been evaluated in a series of canine experiments by means of a direct hormone stimulation test. No reduction of the basal or stimulated exocrine pancreatic secretion was noted after this type of vagotomy.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Pancreatic Function after Seromyotomy of the Canine Stomach

Hee¹,

Verhulst²,

Schil³

1988

Eur Surg Res

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“…[34][35][36][37][38] Although the enterohepatic circulation was interrupted, the bile acid pool was maintained by continuous infusion of Na ϩ -taurocholate at a nonsaturating rate. 39 Because previous studies have shown minimal effects of secretin in normal rats, 21,23 in contrast with the significant effects observed in rats with bile ductular cell proliferation, 23,24 high doses of the hormone were tried (Fig.…”

Section: Discussionmentioning

confidence: 99%

Bicarbonate-rich choleresis induced by secretin in normal rat is taurocholate-dependent and involves AE2 anion exchanger

et al. 2006

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Canalicular bile is modified along bile ducts through reabsorptive and secretory processes regulated by nerves, bile salts, and hormones such as secretin. Secretin stimulates ductular cystic fibrosis transmembrane conductance regulator (CFTR)-dependent Cl ؊ efflux and subsequent biliary HCO 3 ؊ secretion, possibly via Cl ؊ /HCO 3 ؊ anion exchange (AE). However, the contribution of secretin to bile regulation in the normal rat, the significance of choleretic bile salts in secretin effects, and the role of Cl ؊ /HCO 3 ؊ exchange in secretin-stimulated HCO 3 ؊ secretion all remain unclear. Here, secretin was administered to normal rats with maintained bile acid pool via continuous taurocholate infusion. Bile flow and biliary HCO 3 ؊ and Cl ؊ excretion were monitored following intrabiliary retrograde fluxes of saline solutions with and without the Cl ؊ channel inhibitor 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) or the Cl ؊ /HCO 3 ؊ exchange inhibitor 4,4 -diisothiocyanatostilbene-2,2 -disulfonic acid (DIDS). Secretin increased bile flow and biliary excretion of HCO 3 ؊ and Cl ؊ . Interestingly, secretin effects were not observed in the absence of taurocholate. Whereas secretin effects were all blocked by intrabiliary NPPB, DIDS only inhibited secretin-induced increases in bile flow and HCO 3 ؊ excretion but not the increased Cl ؊ excretion, revealing a role of biliary Cl ؊ /HCO 3 ؊ exchange in secretininduced, bicarbonate-rich choleresis in normal rats. Finally, small hairpin RNA adenoviral constructs were used to demonstrate the involvement of the Na ؉ -independent anion exchanger 2 (AE2) through gene silencing in normal rat cholangiocytes. AE2 gene silencing caused a marked inhibition of unstimulated and secretin-stimulated Cl ؊ /HCO 3 ؊ exchange. In conclusion, maintenance of the bile acid pool is crucial for secretin to induce bicarbonate-rich choleresis in the normal rat and that this occurs via a chloride-bicarbonate exchange process consistent with AE2 function. (HEPATOLOGY 2006;43:266-275.) S ecretin is known to induce bicarbonate-rich hydrocholeresis in many animal species. 1-7 Its interaction with a G-protein-coupled receptor selectively localized to the epithelial bile duct cells 8 results in increased intracellular levels of cyclic adenosine monophosphate (cAMP) [cAMP] i 7,9,10 and protein kinase A activation. 11,12 Phosphorylation and opening of a cAMP-dependent Cl Ϫ channel, the cystic fibrosis transmembrane conductance regulator (CFTR), 13 causes Cl Ϫ efflux to the ductular lumen. This appears to stimulate an apical Na ϩ -independent Cl Ϫ /HCO 3 Ϫ anion exchange (AE), 14 with HCO 3 Ϫ efflux and Cl Ϫ influx, that is facilitated by the outside to inside transmembrane gradient of Cl Ϫ at relatively high intracellular HCO 3 Ϫ concentration. [10][11][12]15,16 Several bicarbonate transporters, most of them encoded by the SLC4 and SLC26 gene families, 17 have been described to exert AE activity. A decade ago, we localized one of those polypeptides, the SLC4A2 or AE2, 18 to the apical membrane in...

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“…These stimuli have been shown to produce a choleresis but, as pointed out by Pissidis and Bombeck (1973), this could have been caused indirectly by the release of substances from the gastrointestinal tract. In the experiments of Kaminski et al (1974), however, direct vagal stimulation did not appear to cause release of either cholecystokinin or secretin from the gut. Despite the interest in the effects of the vagus nerves on bile formation in dogs, information on such effects is not available from sheep or from other herbivorous animals.…”

Section: Introductionmentioning

confidence: 73%

“…For example, electrical stimulation of the vagus nerves elicited an increase in bile production in the experiments of Tanturi and Ivy (1938), but not in those of Kaminski et al (1974). Shamfeeding or administration of insulin or 2-deoxyglucose has been used in dogs in efforts to increase vagal activity (Fritz and Brooks 1963;Powell ei al.…”

Section: Introductionmentioning

confidence: 99%

Effect of Electrical Stimulation of the Vagus Nerves on Bile Secretion in Anaesthetized Sheep

Pass¹,

Heath²

1976

Aust. Jnl. Of Bio. Sci.

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Bile was collected before and during electrical stimulation of the vagus nerves in acute experiments on sheep with ligated cystic ducts. Most stimuli caused no change in: bile formation, but a 10-V, 10-Hz stimulus caused a slight increase in bicarbonate output. Neither the response to infused secretin nor the maximum rate of bile salt transpoit by liver cells changed during vagal stimulation; It was concluded that the vagal innervation of the liver is not likely to playa major role in the regulation of bile formation in sheep.

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Effect of electrical vagal stimulation on canine hepatic bile flow

Cited by 40 publications

References 0 publications

Pancreatic Function after Seromyotomy of the Canine Stomach

Pancreatic Function after Seromyotomy of the Canine Stomach

Bicarbonate-rich choleresis induced by secretin in normal rat is taurocholate-dependent and involves AE2 anion exchanger

Effect of Electrical Stimulation of the Vagus Nerves on Bile Secretion in Anaesthetized Sheep

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