Acid Secretion In Dogs Research Articles

Oxygen consumption during thiocyanate inhibition of gastric acid secretion in dogs

Oxygen consumption during thiocyanate inhibition of gastric acid secretion in dogs

Effects of cortisone on parietal cells and acid secretion in dogs

1. 1. The effects of 200 mg. of cortisone daily for three weeks upon gastric secretion and parietal cell mass were measured in 6 dogs with Heidenhain pouches, 3 with Pavlov pouches, and 3 with Heidenhain pouches plus antrectomy. 2. 2. The 24-hour secretory volume, free HCl, and total acid were all significantly increased during cortisone treatment in dogs with both innervated and denervated pouches. 3. 3. The antrectomized dogs showed a small but statistically insignificant increment in acid secretion on cortisone treatment. 4. 4. The maximum secretory response to histamine showed a twofold increase during cortisone administration in the 4 dogs so studied. 5. 5. The mean parietal cell population was significantly decreased—13% in dogs with Heidenhain pouches and 17% in dogs with Pavlov pouches. Since an increased secretion of histamine is usually associated with an increase in parietal cell mass, the rise in gastric acid secretion was attributed to an increased parietal cell sensitivity to normal stimuli in cortisone-treated dogs.

Effect of portacaval shunt on gastric acid secretion in dogs with liver disease, portal hypertension and massive ascites.

Effect of portacaval shunt on gastric acid secretion in dogs with liver disease, portal hypertension and massive ascites.

Acid Response to Gastrin and Related Peptides

Summary Histamine, gastrin II, and several peptides related to gastrin were compared as stimulants of gastric secretion of acid in dogs with both Heidenhain pouches and gastric fistulas. The maximal response of the Heidenhain pouch to gastrin and the peptides was lower than to histamine. The maximal response of the gastric fistula (vagally innervated) was about 20% higher with gastrin than with histamine, a finding similar to that reported for the intact stomach of man. Three peptides related to gastrin were studied. These were the C-terminal tetrapeptide of gastrin, Try.Met .Asp.Phe. NH 2 , and the carbamoyl and β-alanyl derivatives of that tetrapeptide. Although all of these peptides were more potent than histamine on a weight basis, none was as potent as gastrin and only the β-alanyl pentapeptide gave a maximal response equal to that of gastrin.

THE EFFECT OF A NEW ANTICHOLINERGIC DRUG, HETERONIUM BROMIDE, ON BASAL GASTRIC SECRETION.

p HARMACOLOGISTS AND CLINICIANS have long recognized the desirability of a drug which would inhibit gastric secretion and motility while producing a nlinimum of other anticholinergic effects such as dryness of the mouth, urinary hesitancy, and blurring vision. Although the ideal compound has not been and may never be found, many new drugs have been developed in the hope that they will, at least in part, have selective activity. Recently a potent new anticholinergic drug, heteronium bromide,* has been shown to possess marked antisecretory and antimotor effects. Heteroniurn-~ as the bromide, dl- (I-methyl-3-pyrrolinyl) -a-phenyl-a- (2thienyl) glycolate methobromide, is a white, crystalline solid that is very soluble in water and alcohol. The structural formula is shown in Fig. 1. The effects of heteronium bromide on gastric acid secretion in rats and dogs in which pyloric ligation has been done was carefully evaluated by Lim a The study in rats was carried out according to the method described by Shay et al. At a dose of 20 mg./kg, administered orally, heteronium bromide and atropine sulfate were compared to a placebo. Heteronium bromide significantly inhibited both the vohune of secretion and free hydrochloric acid output. Atropine sulfate significantly inhibited the volume but did not significantly affect free hydrochloric acid output. The effect of heteronium bromide on meal-stimulated gastric acid secretion in dogs was also studied. The method of the study and the dogs' reFrom the Lilly Laboratory for Clinical Research, the Gastro-Intestinal Clinic, Marion County General Hospital, and Indiana University School of Medicine, Indianapolis, Ind. The authors express their appreciation to the staff of the Lilly Laboratories for Clinical Research; the nursing staff, for their careful collection of samples; Mr. Jacque Ferguson for the meticulous analysis of the samples; and the medical staff, Mrs. Nellita Sumner. and Mrs. Hilda Banks, for their help and cooperation in this study. *Eli Lilly and Company, Indianapolis, Ind. tThe generic name heteronium has recently been assigned to the active principle in heteroninm bromide. There is 0.8 rag. of heteronium in I rug. of heteronimn bromide.

CONCENTRATION OF AMMONIA IN THE GASTRIC VENOUS BLOOD OF DOGS DURING ACID SECRETION.

AMMONIA has been detected in gastric juice during acid secretion in response to parenteral histamine in many species, including man and dog1–4. This has been attributed to the action of urease in the gastric mucosa on endogenous urea4,5. Conflicting observations have been made as to whether ammonia is also released into gastric venous blood during acid secretion6,7. Turner8 found a rise in arterial ammonia concentration 30–60 min after histamine in those cirrhotic patients with a previous history of hepatic coma or pre-coma, but not in cirrhotic patients without such a history. He suggested that the origin of this rise might possibly be related to gastric secretion. A further attempt has therefore been made to determine whether ammonia is released into the venous blood leaving the stomach during, or after, histamine stimulated acid secretion in dogs.

Gastric acid secretion in dogs during pregnancy and lactation.

Gastric acid secretion in dogs during pregnancy and lactation.

Inhibition of gastric secretion of acid in dogs by carbonic anhydrase inhibitor, 2-acetylamino-1, 3, 4-thiadiazole-5-sulfonamide.

Inhibition of gastric secretion of acid in dogs by carbonic anhydrase inhibitor, 2-acetylamino-1, 3, 4-thiadiazole-5-sulfonamide.