In 9 conscious dogs (4 of whom were alcohol-fed for 24 months with 50% intragastric ethanol), provided with gastric and duodenal fistulae (Thomas cannula), the effects were studied of an acute iv ethanol infusion (1.3 g/kg) on hepatic bile secretory plateau levels after emptying of the gallbladder was induced by a continuous perfusion of secretin (0.5 CU/kg/hr) plus CCK-PZ (8 Crick-Harper-Raper U/kg/hr) and sodium taurocholate (0.62 mumol/kg/min). Acute iv ethanol infusion in nonalcoholic dogs reduced hepatic bile flow rate (29%), bile salt concentration (55%) and output (67%). In alcohol-fed dogs, acute iv ethanol reduced only the rate of flow (25%). Hepatic bile salt concentration and output plateau values were significantly higher in the alcohol-fed than in the nonalcoholic dogs. There were no significant differences between the two groups of dogs in the rate of evacuation, bile salt output, or lipid composition of gall bladder bile following a single iv injection of CCK-PZ.

Animals↗

PubMed1976

[Needle aspiration biopsy as a new method of intraoperative diagnosis of pancreatic neoplasms].

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Biopsy, Needle↗

PubMed1976

[The physiopathology of the external pancreatic secretion (author's transl)].

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Cholecystokinin↗

PubMed1976

Evidences for duodenopancreatic reflexes and an anti-CCK factor with lidocaine infused intravenously and sprayed topically on pancreatic papilla in nonalcoholic and alcohol-fed dogs.

In 14 duodenal Thomas fistula dogs, four of them alcohol-fed for two years, lidocaine, applied topically to the duodenal pancreatic papilla, inhibited secretin-induced pancreatic secretion probably by interrupting duodenopancreatic reflexes that contribute to the "pancreon's" cholinergic tone. Opposite effects were observed with lidocaine administered against a CCK plus secretin background stimulation of the pancreas. The significant rising of volume and protein output above plateau levels were enhanced by chronic alcohol feeding. Lidocaine infused intravenously did not change secretin-induced pancreatic secretion but raised CCK and secretin evoked plateau secretion levels. Chronic alcoholism enhanced these latter effects. Atropine perfusion superimposed on CCK and secretin stimulation did not prevent but raised the intravenous lidocaine-induced pancreatic secretion changes. It is postulated that the modifications elicited by lidocaine sprayed topically and infused intravenously on CCK plus secretin evoked pancreatic secretion plateau levels are due to depression of an anti-CCK factor secreted by the small intestine mucosa.

Administration, Topical↗

PubMed1976

Reserpine-induced dissociation of canine pancreatic secretion.

In five dogs, provided with chronic pancreatic and gastric fistulas (Thomas' cannula), the effects on exocrine pancreatic secretion of an intravenous continuous perfusion of gastrin (Eurorga, hog gastrin I-II, 6 mug./kg./hr.) and secretin (GIH, 0.5 C.U./kg.hr.) was studied before and after 48 hours of reserpine treatment (0.1 mg./kg./24 hr.). When compared with the pretreated plateau levels, reserpine induced a significant pancreatic secretion dissociation, a depressive of the alkaline and a rising of the protein component. The former phenomenon suggests a participation of a catecholamines in the secretin-elicited pancreatic electrolyte secretion. The latter, an enhanced sensitivity of intranpancreatic and/or acinar cells of the "pancreon" to gastrin stimulation.

Animals↗