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Biomedical subjects

J H Baron

Publications and source records attributed to J H Baron.

At least 163 records · Page 9Linked to original sources
PubMed1979

The effect of salbutamol and propranolol on pentagastrin, histamine and meal-stimulated acid and pepsin secretion in the dog.

The beta 2 adrenergic agonist Salbutamol was infused intravenously in doses of 0.05, 0.1 and 0.2 microgram/kg-min in conscious dogs with gastric fistulae. Salbutamol inhibited meal-stimulated acid (measured with intragastric titration) by up to 82%. Salbutamol produced dose-related inhibition of acid stimulated by pentagastrin (up to 88%) and by histamine (up to 52%). Pepsin secretion in response to histamine (but not pentagastrin) was also inhibited by salbutamol. The salbutamol infusion caused a marked tachycardia, an increase in pulse pressure, slight hyperkalaemia and hyperglycaemia. The beta-adrenergic antagonist propranolol augmented pentagastrin-stimulated acid and inhibited meal-stimulated secretion. Propranolol abolished salbutamol - induced tachycardia, and blocked the inhibition by salbutamol of pentagastrin-stimulated acid. Salbutamol inhibition of acid in the dog provides further support for the hypothesis that there are beta 2-adrenergic receptors in the stomach.

Albuterol↗
PubMed1978

Inhibition of pancreas and gallbladder by pancreatic polypeptide.

Stimulated pancreatic and biliary outputs were studied in seven healthy subjects during intravenous infusion of bovine pancreatic polypeptide (P.P.) (mean dose 65 pmol/kg/h). P.P. significantly inhibited outputs of trypsin and bilirubin at plasma concentrations similar to those observed after meals. In four cholecystectomised subjects, P.P. inhibited only trypsin output.

Adult↗
PubMed1978

Inhibition by somatostatin (growth-hormone release-inhibiting hormone, GH-RIH) of gastric acid and pepsin and G-cell release of gastrin.

Somatostatin (cyclic growth-hormone release-inhibiting hormone--GH-RIH) was infused into dogs with gastric fistulae. Somatostatin inhibited gastric acid response to four gastric stimulants--insulin, food, histamine, and pentagastrin. Histamine- and pentagastrin-stimulated pepsins were inhibited similarly to inhibition of acid. Somatostatin inhibited the gastrin response to insulin and food.

Animals↗
PubMed1978

Serum carbenoxolone in patients with gastric and duodenal ulcer: Absorption, efficacy and side-effects.

The absorption of carbenoxolone sodium has been studied in 15 patients with gastric ulcer and eight patients with duodenal ulcer treated for four weeks. Blood levels of carbenoxolone showed a log distribution, varied markedly between patients, and were significantly higher after Biogastrone tablets (300 mg/day) than after Duogastrone capsules (200 mg/day). Serum carbenoxolone levels were similar in patients taking Biogastrone tablets before or after meals, and in patients taking Biogastrone tablets or Duogastrone capsules with or without antacids following chronic administration. Serum carbenoxolone levels were similar in patients whose gastric ulcers had or had not healed after four weeks' treatment. Serum carbenoxolone was significantly higher in patients who developed oedema, and was significantly correlated with age and with fall in plasma potassium. Carbenoxolone may exert its metabolic effects systemically, but its ulcer-healing effects topically; additional studies are needed to test this hypothesis.

Adult↗
PubMed1978

Twenty-four hour gastric acidity after vagotomy.

Twenty-four hour intragastric pH during normal daily activity has been studied by nasogastric intubation and aspiration of gastric samples in seven patients four years after vagotomy (four truncal, three selective). Two of these patients also had pre- and early postoperative studies. Mean pH was inversely correlated with basal, insulin- and pentagastrin-stimulated acid outputs. However, one of four patients after truncal vagotomy with drainage, and two of three after selective vagotomy and drainage had most of their hourly intragastric pH values more acidic than pH 3.5 despite more than 70% reductions in preoperative stimulated-acid outputs.

Gastric Acidity Determination↗
PubMed1978

G cell population of the gastric antrum, plasma gastrin, and gastric acid secretion in patients with and without duodenal ulcer.

Estimates of the G cell population were made in 24 resected human pyloric antra from counts of cells in multiple samples and from measurements of antral size. Measurements had been made previously in 20 subjects of acid output (basal and after pentagastrin) and in 10 subjects of plasma gastrin (basal and after insulin + bicarbonate). G cells were most dense near the pylorus, but their circumferential distribution was even. The G cell populations ranged from 8 to 15 (mean 10) million in four control patients and from 3 to 43 (mean 18) million in 15 patients with duodenal ulcer. Those with recurrent ulcer after vagotomy had either a low G cell count and incomplete vagotomy, or a high G cell count and apparently complete denervation. Two patients with hypergastrinaemia and duodenal ulcer had moderate (29 X 10(6)) or marked (56 X 10(6)) excesses of G cells. 'G cell hyperplasia' may represent the extreme end of the normal range of G cell numbers in the antrum, and can be assessed by semi-quantitative grading of G cell hyperplasia in antral biopsies. There were significant direct correlations between antral area and G cell density, between peak acid output and G cell population, and between basal plasma gastrin and G cell density (but not population). We suggest that, in patients with duodenal ulcer, acid and gastrin secretion are interrelated and that both are related to the masses of parietal cells and of G cells.

Cell Count↗
PubMed1978

Effect of bovine pancreatic polypeptide on gastric acid and pepsin output in man.

Bovine pancreatic polypeptide was infused intravenously in 16 healthy volunteers at a mean dose of 218 pmol/kg/hr, producing plasma levels similar to those after meals. Basal and pentagastrin-stimulated acid and pepsin outputs and plasma gastrin concentrations were unchanged by BPP. Pancreatic polypeptide is unlikely to be an important physiological modulator of these secretions in man.

Adult↗
PubMed1977

Peptic ulceration, gastric secretion, and renal transplantation.

Fifty-four patients on haemodialysis for chronic renal failure underwent renal transplantation. Basal and maximum acid output and the incidence of peptic ulcer before transplantation were not significantly different from those of controls. But after renal transplantation the incidence of symptoms of peptic ulcer was high (22%) and four out of six patients who developed gastrointestinal bleeding died from this complication. In men peak acid output was significantly increased after renal transplantation and was associated with a 30% incidence of symptoms of peptic ulcer compared with 10% in women, who showed no significant change in mean basal or peak acid output. Peptic ulceration after transplantation was not associated with steroid dosage, hyperparathyroidism, or the height of blood urea concentrations. Given criteria of a history of dyspepsia, abnormal barium meal findings, or gastric hypersecretion, it was not possible to identify patients at risk from peptic ulceration or life-threatening complications after renal transplantation. Thus the routine screening of these patients for peptic ulcer has no practical value, and the incidence of fatal complications is not high enough to justify routine prophylactic anti-ulcer surgery aimed at reducing acid secretion before renal transplantation.

Female↗
PubMed1977

Secretagogue-produced duodenal ulcers in the rat.

Duodenal ulcers were produced in rats by the subcutaneous infusion for 6-48 hours of two gastric secretagogues in combination: pentagastrin (2 or 4 microgram kg-1 min-1) and carbachol (0-4 or 0-8 microgram kg-1 min-1). With increasing duration of infusion and higher doses there were increases in the incidence, severity, number and perforation rate of duodenal ulcers, their caudad distribution and mortality from peritonitis. This method of producing duodenal ulcers may sufficiently resemble the clinical situation to provide a model for the study of anti-ulcer drugs and the natural history of duodenal ulcers.

Animals↗
PubMed1977

Morphological and pharmacological studies of the parietal cells of the stomach in the dog during periods of maximal acid output and after the gastric secretory inhibitor UK-9040.

UK-9040, a derivative of the antihistamine triprolidine, is a potent gastric secretory inhibitor. Given orally to dogs it reduced gastric acid, pepsin and volume output in response to food, insulin, histamine, N-methyl histamine, and pentagastrin. Doses of 6-36 mg/kg administered orally four to five hours before the secretagogues produced a dose-dependant and up to 100% inhibition in the outputs of innervated gastric fistula and denervated Heidenhain pouch. Inhibition was still present 24 hours after administration of UK-9040 but was absent at 48 hours. Blood pressure and pulse rate were not affected. Studies with the electron microscope revealed that the normal ultrastructural responses to gastric secretory stimulation were arrested. UK-9040 showed no cumulative effect, tolerance did not occur, and after withdrawal of the drug the physiological and morphological gastric responses of the parietal cells rapidly returned to normal.

Animals↗
PubMed1977

Gastrin, antral g cells, and gastric acid in secretagogue-induced and antihistamine-inhibited duodenal ulcers.

In fasting control rats there was continuous basal gastric acid secretion, with a low plasma gastrin and antral G-cells full or immunofluroescent gastrin. After subcutaneous infusion of the gastric secretagogues, pentagastrin + carbachol, there was a six-hour period of gastric hypersecretion, but no change in plasma and G-cell gastrin. Pretreatment with the antihistamine derivative, Pfizer UK-9040, decreased both basal and stimulated acid secretion, whereas plasma gastrin levels increased and the antral G-cells were emptied of gastrin. These results suggest that this antihistamine derivative decreases gastric acid secretion by a direct action on the parietal cells and not by reducing gastrin release from the G-cells. The increased release of gastrin from the G-cells may be secondary to decreased gastric acid production, or more probably by a direct stimulation of the antral G-cells.

Animals↗
PubMed1976

Medical treatment of gastric and duodenal ulcer.

Antacids prove ready if only temporary relief of the symptoms of ulcers. Physicians have been able to increase the rate of healing of gastric ulcers by advising patients to stop smoking and then either admit them to hospital for bed-rest, or use carbenoxolone sodium as an outpatient therapy. The early trials of some other drugs have shown increase in rate of healing of gastric ulcer, but there is no medical treatment which will prevent the high recurrence rate of benign gastric ulcer. The limited data indicate that adequate medical reduction in acid secretion and enhancement of mucosal resistance may benefit patients with duodenal ulcer.

Antacids↗