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Biomedical subjects

J H Baron

Publications and source records attributed to J H Baron.

At least 145 records · Page 8Linked to original sources
PubMed1982

Current views on pathogenesis of peptic ulcer.

In duodenal ulcer disease, peptic digestion and ulceration of the duodenal mucosa can be related to increased duodenal acidity, which in about half the patients is due to inherited gastric hypersecretion, with too many parietal and chief cells. The others, normosecretors, may have parietal and chief cells excessively stimulated by, and/or specially sensitive to, gastrins and the vagus, together with inadequate suppression of the release of antral gastrin and the secretion of gastric acid. The abnormality is gastric hypersecretion with inappropriate hypergastrinaemia. The reserve capacities of the duodenal defence mechanisms are probably normal, but there seems to be a functional impairment with inadequate defence by decreased bicarbonate secretion into the duodenum, but as yet no clear impairment of the release of mucosal hormones. There are marked hereditary factors in gastric ulcer too. Some ulcers are related to gastric irritants (salicylates, tobacco). Oi's anatomical dual-control mechanism explains why gastric ulcers are usually solitary and at one site. Gastritis and duodenal reflux are probably the most important factors in type 1, body ulcers. Gastric stasis may be a factor in type 2, combined ulcers. Type 3 prepyloric ulcers resemble duodenal ulcers, both in blood group and hypersecretion.

Duodenum↗
PubMed1980

Effect of neurotensin on gastric function in man.

Neurotensin is a peptide recently discovered in the human ileum and it is released into plasma after ingestion of food. Neurotensin was infused intravenously into 12 healthy volunteers at a mean dose of 2.4 pmol/kg/min, the mean rise in plasma levels being 89 +/- 8 pmol/l. An inhibition of both gastric acid and pepsin output, and also a delay in gastric emptying of oral glucose, were observed. Neurotensin may therefore have a physiological role in modulating gastric function in man.

Adult↗
PubMed1980

Eating and ulcers.

Explore the source record for details and available documents.

Dietary Fiber↗
PubMed1980

Exogenous and endogenous acid and pepsins in the pathogenesis of duodenal ulcers in the rat.

A continuous subcutaneous infusion for 24 hr of the gastric secretagogues, pentagastrin (4 micrograms/kg/min) together with carbachol (0.8 micrograms/kg/min) produced a 100% incidence of duodenal ulcers (DU) in male albino Wistar rats. The mean acid output producing these duodenal ulcers was 2.3 mmol/24 hr, with a gastric secretory volume of 25 (+/- 1) ml/24 hr at an acid concentration of 91 (+/- 2) mmol/liter. The pepsin activity in the gastric juice was 185 micrograms/ml. To simulate this acid-pepsin hypersecretion, acid and/or pepsin was infused intragastrically for 24 hr. The intragastric infusion of hydrochloric acid (0.1 M, 0.2 M, 0.5 M) alone and hog purified pepsin (2.5, 5, 10 mg/24 hr) at a constant rate of 1 ml/hr for 24 hr failed to produce duodenal ulcers in rats although gastric lesions in the body of the stomach were produced. The infusion of 0.2 M HCl with 5 mg pepsin over 24 hr produced DU in two of 10 rats. However, pooled secretagogue-stimulated gastric juice, infused intragastrically, produced DUs in 11 of 12 rats. Acid alone does not produce DU experimentally in rats at the rate of infusion used in these experiments. Acid and exogenous procine pepsin (similar to human pepsin 3 on agar gel electrophoresis) rarely produced duodenal ulcers. However, acid and endogenous rat pepsin are needed together for the duodenal ulcerogenesis. This pepsin may be an obligatory ulcerogenic factor in the rat.

Animals↗
PubMed1980

Malabsorption and macroamylasemia. Response to gluten withdrawal.

A 36 year old woman presented with malabsorption and macroamylasemia. The macroamylase was characterized and shown to be a complex of pancreatic amylase and immunoglobulin A(IgA). The patient had the clinical and histologic features of adult celiac disease, and responded to a gluten-free diet. The macroamylase complex disappeared from the serum after gluten withdrawal, a hitherto unreported finding in the syndrome of malabsorption and hyperamylasemia.

Adult↗
PubMed1980

The effect of pirenzepine on meal-stimulated gastrointestinal hormones.

The effects of pirenzepine on the plasma concentrations of gut hormones in the fasting and postprandial states were studied in six healthy subjects. On separate days and in random order, 10 mg pirenzepine, in 2 ml of solvent, or 2 ml saline (0.15 mol/l) were given intravenously 30 min before a standard normal breakfast (2220 kJ). Pirenzepine was not found to affect basal or postprandial levels of insulin, glucagon, gastric inhibitory peptide (GIP), neurotensin, vasoactive intestinal peptide (VIP) or somatostatin. The basal concentration of pancreatic polypeptide (PP) was lowered (p less than 0.05) and the postprandial elevation reduced, though not significantly. While the basal concentration of motilin was also suppressed (p less than 0.05), the postprandial elevation remained unchanged following pirenzepine. The release of enteroglucagon was reduced significantly in the basal and postprandial states (p less than 0.05 and p less than 0.025 respectively). The postprandial gastrin response was prolonged slightly, but insignificantly, by pirenzepine. It is concluded that pirenzepine does not exert any major or unexpected actions on the hormonal control of digestion.

Adult↗
PubMed1980

Influence of intravenous pirenzepine on gastric acid and pepsin in man.

Patients with dyspepsia were asked to volunteer for two gastric secretion tests preceded by a single intravenous injection of pirenzepine 10 mg in the one and 0.9% saline in the other (in random order). In each test gastric secretion was aspirated continuously. 0.9% saline was infused intravenously for 30 minutes followed by insulin 0.15 micrograms/kg-h for 90 minutes, saline for 30 minutes and finally pentagastrin for 90 minutes in doses of either 6, 1, 0.5 or 0.25 micrograms/kg-h. Gastric samples were analysed for volume, pH, titratable acidity and pepsin. Basal outputs of acid and pepsin were not altered by pirenzepine. Insulin-stimulated acid output was significantly reduced (p less than 0.05) from a mean of 32.7 to 22.6 mmol/h (-31%). The mean percentage reduction was 16%. Acid and pepsin outputs after pentagastrin 0.25-6 micrograms/kg-h were not significantly altered by this dose of pirenzepine.

Adult↗
PubMed1980

Serum carbenoxolone: ulcer-healing and metabolic effects.

The relationship of serum carbenoxolone to dosage, age, sex, efficacy and side-effects were studied in 92 patients. Log serum carbenoxolone was correlated with dose and with age, and was higher in women. Serum levels were not significantly different in those patients with duodenal (or gastric) ulcer whose ulcers had or had not healed after allowance was made by analysis of variance for the effects of age and sex. However, oedema and hypokalaemia were associated with higher serum levels. These results support the concept that the ulcer-healing effect of carbenoxolone is topical rather than systemic.

Adult↗
PubMed1980

The influence of amiloride on the therapeutic and metabolic effects of carbenoxolone in patients with gastric ulcer. A double-blind controlled trial.

Patients with benign gastric ulcer were treated for four weeks with carbenoxolone sodium as Biogastrone tablets 100 mg three times a day, and if the ulcers were not healed at 4 weeks treatment was continued for a further 4 weeks. Fifty two patients entered the trial, and 12 were withdrawn. In 17 patients who were randomly allotted double-blind additional dummy tablets 16 of their ulcer healed completely endoscopically, whereas of the 23 patients given additional amiloride 5 mg three times a day only 14 ulcers healed, a significant reduction in ulcer healing. The clinical (weight gain and oedema) and metabolic (hypertension, hypokalaemia and hypernatraemia) side-effects were reduced by the active amiloride therapy, but serum carbenoxolone levels were not affected. Thus the potassium-retaining diuretic amiloride, like the aldosterone antagonist spironolactone, markedly reduces both the ulcer-healing and the metabolic side-effects of carbenoxolone sodium, and should not be used together with it in the treatment of peptic ulcer.

Adult↗
PubMed1979

Effect of bovine pancreatic polypeptide on basal pancreatic and biliary outputs in man.

Basal pancreatic and biliary outputs were examined in seven healthy volunteers during intravenous infusion of bovine pancreatic polypeptide (BPP) at a mean dose of 320 pmol/kg/hr. BPP significantly (P less than 0.02) inhibited outputs of trypsin and bilirubin, without affecting bicarbonate. These studies suggest the possibility that pancreatic polypeptide may have a role in the regulation of biliary and pancreatic enzyme secretion in man.

Adult↗
PubMed1979

Cimetidine and salbutamol combined inhibition of gastric acid secretion in the dog.

The effects of salbutamol and cimetidine, alone and in combination, on pentagastrin-stimulated gastric secretion have been studied in conscious dogs with gastric fistulae. Salbutamol 24 nmol/kg.h alone and cimetidine 4 mumol/kg.h alone inhibited acid up to 69%, cimetidine 8 mumol/kg.h produced up to 87% inhibition and the combination of cimetidine 4 mumol/kg.h and salbutamol 24 nmol/kg.h almost totally inhibited acid (up to 99%). The pharmacokinetics of these inhibitions were studied and salbutamol and/or cimetidine caused a complex uncompetitive inhibition of pentagastrin-stimulated acid. The inhibitory combination of the two drugs was additive.

Albuterol↗