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Biomedical subjects

J I Isenberg

Publications and source records attributed to J I Isenberg.

At least 127 records · Page 7Linked to original sources
PubMed1976

The effect of various forms of milk on gastric-acid secretion. Studies in patients with duodenal ulcer and normal subjects.

Milk is commonly recommended as therapy for patients with peptic ulcer. The purpose of this study was to examine the effect of various forms of milk and 0.15 M NaCl (control) on gastric-acid secretion in five patients with duodenal ulcer during a period of remission and in five normal subjects. A significant (P less than 0.05) increase in acid secretion in both groups was produced by 240 ml of whole, low-fat, and nonfat milk. The acid secretory responses to milk were equivalent to approximately 20% to 35% of maximal betazole - or pentagastrin-stimulated acid output. Gastric-acid secretion produced a significant (P less than 0.05) increase in acid secretion in the patients with duodenal ulcer but not in the normal subjects. Because milk contains both protein and calcium, and each are stimulants of gastric-acid secretion, there is reason to question its frequent ingestion by patients with peptic ulcer.

Animals↗
PubMed1976

The effect of 16,16-dimethyl prostaglandin E2 on meal-stimulated gastric acid secretion and serum gastrin in duodenal ulcer patients.

The effect of intragastric and intraduodenal 16,16-dimethyl prostaglandin E2 (dm PGE2) on meal-stimulated gastric acid secretion and gastrin release was studied in patients with inactive duodenal ulcer. Compared to placebo, doses of 0.75, 1.00, 1.33, and 1.77 mug per kg of dm PGE2 instilled into the stomach inhibited meal-stimulated gastric acid secretion by 61 to 94% (P less than 0.01). The 1.00, 1.33, and 1.77 mug per kg doses inhibited acid secretion significantly (P less than 0.05) more than an optimal dose of propantheline bromide. Intragastric dm PGE2 (1 mug per kg) was significantly (P less than 0.05) more effective than intraduodenal dm PGE2 (1 mug per kg) in inhibiting both gastric acid secretion and gastrin release. After 1.33 and 1.77 mug per kg, some patients experienced abdominal cramps, or diarrhea, or both, but at doses of 1.00 mug per kg or less no apparent untoward side effects were observed. It is concluded that 16,16-dm PGE2 significantly inhibits meal-stimulated gastric acid secretion and gastrin release, and may be of therapeutic value in patients with peptic ulcer provided it is free of untoward side-effects with chronic administration.

Duodenal Ulcer↗
PubMed1976

Cimetidine inhibits caffeine-stimulated gastric acid secretion in man.

In animals, gastric acid secretion stimulated by the methyl xanthine, theophylline, was not inhibited by histamine H2-receptor antagonists. In this study the effect in man of the H2-receptor antagonist, cimetidine, on gastric acid secretion stimulated by the methyl xanthine, caffeine, was examined. Caffeine was given intravenously for 2 hr in a dose of 9 mg per kg-hr to 5 patients with duodenal ulcer and 5 normal subjects. Three hundred milligrams of cimetidine administered orally 30 min before the start of the caffeine infusion completely abolished the acid secretory response in all subjects, decreasing acid secretion to less than basal rates. It is concluded that in man the H2-receptor antagonist, cimetidine, abolished the acid secretory response to the methyl xanthine, caffeine.

Adult↗
PubMed1976

Effect of gastrin on pancreatic enzyme secretion and gallbladder emptying in man.

This study was designed to assess the effect of unsulfated synthetic human little gastrin (HG-17-I) on pancreatic secretion and gallbladder emptying in man. During continuous gastric and duodenal aspiration, 6 male subjects were given, on different days, either HG-17-I (7, 20, 60, 180 AND 540 PMOL KG-1 HR-1), chlecystokinin (0.1, 0.3, and 0.9 UKg hr-1) or 238 pmol kg-1 (500 ng kg-1) of HG-17-I as a rapid intravenous injection. Trypsin output and bilirubin output increased significantly (P less than 0.05) above basal levels during the infusion of both peptides. During HG-17-I infusion the highest trypsin output (2.08 +/- 0.22 Karmen U per 10 min) and bilirubin output (4.66 +/- 0.61 mg per 10 min) occurred during the 60 pmol kg-1 hr-1 dose, whereas highest acid output occurred during the 540 pmol kg-1 hr-1 dose. Rapid intravenous injection of HG-17-I produced a prompt and significant rise in trypsin, bilirubin, bicarbonate, and acid outputs. It is concluded that HG-17-I produced significant pancreatic enzyme secretion and gallbladder emptying at doses that are submaximal for acid secretion, suggesting that this may be a physiological effect of gastrin.

Adult↗
PubMed1975

Inhibition of gastric acid secretion by cimetidine in patients with duodenal ulcer.

Cimetidine, a non-thiourea-containing H2-receptor antagonist, was studied in seven patients with duodenal ulcer. Oral doses of 100, 200, and 300 mg were tested. Each dose significantly inhibited basal and meal-stimulated secretion. After 300 mg, basal acid secretion was essentially zero for at least five hours. The meal-stimulated three-hour acid output after the 300-mg dose was reduced by 67%. Cimetidine, 300 mg, decreased meal-stimulated acid secretion significantly more than an optimal effective dose of propantheline bromide (P less than 0.05). Inhibition of meal-stimualted gastric acid secretion showed a significant relation to peak blood cimetidine concentration (r is equal to 0.76, P less than 0.01). Cimetidine did not affect meal-stimulated gastrin release. No toxicity was observed after serial doses given during these tests. Cimetidine may be useful in treatment of acid-peptic diseases provided no important toxicity appears on chronic testing.

Administration, Oral↗
PubMed1975

Peptic ulcer disease.

Smoking, heredity, aspirin ingestion, and various diseases are associated with increased prevalence of peptic ulcer disease. Significant pathophysiologic differences between ulcer patients and normal subjects have been shown to exist, but many of the observed abnormalities are still poorly understood and require further study. Prospective studies are also needed to quantitate the role of psychologic factors in the pathogenesis of ulcer disease. Ulcer disease is diagnosed by history, physical examination, upper gastrointestinal radiography, and endoscopy. In some patients measurements of serum gastrin levels and gastric acid secretion at rest and after stimulation give significant information. Antacids and anticholinergics remain the primary therapeutic agents; new therapeutic agents are currently under study.

Antacids↗
PubMed1975

The effect of glucagon on barium-enema examination.

Fifty barium-enema studies were performed with glucagon and 50 with a placebo to compare their effect on colonic spasm, patient discomfort, and diagnostic quality. Each drug was administered in a randomized double-blind fashion and was injected intramuscularly 10 minutes before beginning the enema. Bowel relaxation during fluoroscopy was graded. Patients were questioned about discomfort during and immediately after the enema, and radiographs were reviewed blindly for diagnostic quality and degree of spasm. Studies done with glucagon produced significantly less spasm and discomfort and better diagnostic quality compared to the placebo (p less than 0.01).

Barium Sulfate↗
PubMed1975

Increased sensitivity to stimulation of acid secretion by pentagastrin in duodenal ulcer.

The effect of graded doses of pentagastrin (2.7-6,000 ng/kg times h) on gastric acid secretion was measured in 20 duodenal ulcer (DU) and 20 non-DU subjects. Confirming many previous studies, the mean observed highest response and the mean calculated maximal response were significantly greater in DU than in non-DU subjects. The mean dose (plus or minus SE) in ng/kg times h for half maximal response, calculated from responses corrected for basal secretion and normalized for maximal secretion, was 92.1 plus or minus 1.7 in DU and 246.8 plus or minus 24.6 in non-DU subjects, a significant difference. By parallel line bioassay non-DU subjects required 2.8 times more pentagastrin (95% confidence limits 2.1-3.7) than DU highest response. Thus, this study shows that, compared with non-DU subjects, DU patients not only secrete more acid in response to stimulation by pentagastrin but also are more sensitive to stimulation by pentagastrin, that is, need smaller doses to achieve the same fraction of maximal response.

Adult↗