D. F. Magee

The Zinc Content of Bile and Pancreatic Juice in Zinc-Deficient Swine

Abstract The content of zinc, magnesium, calcium, bilirubin, and bile acids was determined in the hepatic bile of zinc-deficient and control swine. Zinc deficiency was produced by dietary zinc restriction while pair fed zinc supplemented animals served as controls for observations of hepatobiliary functions. Pigs weighing 5 kg were placed in two groups and fed the respective diets for 6 weeks; hair and skin abnormalities as well as decreased weight gain were present in the zinc-deficient group by this time. Hepatic bile and pancreatic juice were obtained from each animal after careful isolation and cannulation of the pancreatic and bile ducts. Animals were studied for a 3-hr period while under constant secretin stimulation and chloralose anesthesia. During this period, there was a progressive decrease in the biliary concentrations of bilirubin, bile acids, and magnesium in the bile of both groups, while zinc and calcium levels were not altered. The zinc concentrations in pancreatic juice were reduced in the zinc-deficient animals. The zinc content of the serum, liver, kidney, and pancreas was also decreased in this group. The calcium and magnesium content of the serum and organs was similar in the two groups with the exception of decreased magnesium in the kidney of the zinc-deficient pigs. Low content of zinc in the liver and serum of the deficient animals was associated with a zinc concentration in the bile comparable to the control group; however, the relative content of zinc in pancreatic secretion and bile was found to be altered in zinc deficiency. In control animals 60% of the zinc is in the pancreatic secretion and 40% in the bile. These percentages are reversed in zinc-deficient animals in which 60% of the zinc is derived from the bile.

Adrenergic activity and gastric secretion.

Summary Isoproterenol infusions depress pentagastrin (PG)-stimulated secretion of acid and pepsin from both gastric fistulae and denervated (Heidenhain) pouches in conscious dogs. It was not found to do so if methacholine replaced gastrin. Propranolol reversed the isoproterenol depression of PG stimulation but had no effect on isoproterenol plus methacholine except on the fistula where both acid and pepsin were depressed. It is felt that PG and methacholine act by differing mechanisms both on chief and parietal cells.

Comparison of the action of cholinomimetics and pentagastrin on gastric secretion in dogs

1 Stimulation of acid secretion by muscarinic cholinomimetic agents depended on the periodic interdigestive activity of the stomach. This explains the peak and following fade. 2 Pentagastrin stimulated gastric secretion after a fixed interval and did not depend on the interdigestive activity. 3 Neither gastrin nor methacholine directly contracted the gallbladder in the doses used. 4 A sustained secretion of gastric acid and pepsin, such as follows a meal, required both hormonal stimulation and gastric distension. 5 The magnitude of the acid response from Heidenhain pouches following meals suggested that pentagastrin doses commonly used experimentally greatly exceed the physiological.

The action of intravenous ethanol on gastric secretion.

Summary In conscious dogs, intravenous infusion of ethanol stimulated gastric acid secretion both from the gastric fistula and from the Heidenhain pouch and stimulated pepsin secretion from the fistula but not from the pouch. Acute cervical vagal block with infiltration anesthesia had no effect on ethanol-stimulated gastric secretion. After ganglionic blockade (pentolinium tartrate) ethanol stimulated neither acid nor pepsin secretion from the fistula. Ethanol did not stimulate gastric secretion when the antrum was acidified with 0.1 N HCl. From these experiments, it was concluded that intravenous ethanol stimulated gastric secretion in the main by liberating antral gastrin.

Acetylcholine and Gastric Secretion

Summary Hemicholinium in conscious dogs with gastric fistulae and Heidenhain pouches depressed PG and 2 deoxy-D-glu-cose stimulation of acid and pepsin secretion. On the other hand, it either augmented or did not significantly change histamine- and pilocarpine-promoted secretion. These results support the view that acetyl-choline is an obligatory mediator of the action of PG at secretory effector sites.

Pyloric antral inhibition of gastrin release

Inconsistencies and omissions in current explanations for the well known depressions of gastric acid secretion and blood gastrin levels following acidification by antral stimulants are discussed. Evidence is presented which favors a reciprocal sensitivity relationship between the fundic mucosa and the antral G cells, such that blood gastrin levels rise when the secreting fundic mucosa is compromised and acid secretion in response to exogenous gastrin is increased when G cells are depressed or reduced. The functional connections between the two phenomena are considered to be nervous.

Relationship of periodic pancreatic secretion and gallbladder contraction to plasma cholecystokinin in dogs

SummaryTHE role of cholecystokinin (CCK) on the periodic pancreatic secretion and gallbladder contraction was studied in fasting conscious dogs. The bile pressure peak preceded the pancreatic protein peak by about 30 min. Its pressure at the peak was significantly higher than at the pancreatic peak, while pancreatic protein secretion at the bile peak was significantly lower than at its own peak. Plasma CCK levels at the gallbladder and pancreatic peaks were significantly higher than those at the upper gastrointestinal motor and secretory quiescent period. Levels at either peaks, however, did not differ.Atropine abolished the periodic increase of pancreatic secretion, gallbladder contraction and plasma CCK. It is concluded that the inter-digestive CCK release is dependent on cholinergic nerves. It may modulate the action of the nerves on the pancreas and the gallbladder. Correlation between plasma CCK and pancreatic polypeptide was not significant.

Action of amino acids on stomach, pancreas, and gallbladder in dogs.

SummaryAn intravenous infusion of a 3% solution of amino acids was given to 8 dogs, all with Heidenhain pouches and gastric fistulae. Four of these had duodenal cannulae opposite the pancreatic and 4 opposite the biliary ampulla. The usual basal 100 min spontaneous peaking of pancreatic juice volume and protein secretion was seen but peaks were abolished by the amino acid infusion and troughs were slightly elevated, but the total 90 min volume protein and bicarbonate outputs were not different from control. Gastric acid and pepsin secretions were augmented reaching a peak during the first hour with a subsequent decline. The 90 min acid and pepsin output was significantly higher than control. The gallbladder contracted during the first hour and remained thus until the infusion was terminated. This happened even when the duodenum was kept alkaline, but was abolished by ganglionic blockade. During intravenous amino acid infusion the patterns of gallbladder activity and pancreatic secretion resembled those of the post cibal rather than fasting state.

281 – ACTION OF MORPHINE SULPHATE ON STIMULATED GASTRIC SECRETION IN DOGS

In dogs morphine sulphate suppresses both 2-deoxy-D-glucose and pentagastrin-stimulated acid and pepsin secretion, but not histimaine- and pilocarpine-stimulated acid. This is consistent with the view that morphine both depresses acetylcholine release from cholinergic endings in the stomach and that pentagastrin acts by liberation of acetylcholine from these endings.