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Biomedical subjects

A Berstad

Publications and source records attributed to A Berstad.

At least 217 records · Page 12Linked to original sources
PubMed1982

Antacids and pepsin.

In a certain pH range, common antacids containing aluminium hydroxide gel have powerful adsorbent and precipitating effect on pepsin in human gastric juice, but there is no inactivation of pepsin apart from that produced by alteration of pH. In vivo, reduced pepsin concentration in aspirates from the stomach, after oral administration of aluminium hydroxide-containing antacids, may be due to precipitation of pepsin by the antacid within the stomach and the heavier, precipitated material not being withdrawn with the juice through the tube.

Aluminum Hydroxide↗
PubMed1981

Cimetidine treatment of recurrent ulcer after proximal gastric vagotomy.

Twenty-one patients with endoscopically confirmed recurrent ulceration after proximal gastric vagotomy entered an open trial of treatment with cimetidine, 1.0 g/day. Twenty patients completed 6 weeks' treatment, and repeat endoscopy showed ulcer healing in 18 of 20 patients. One patient's ulcer was found to be healed on X-ray examination, and the other patient had a healed ulcer after an additional 2 weeks' treatment. Eighteen of the patients with healed ulcer entered a maintenance trial of cimetidine, 400 mg at night. During the 1-year follow-up period the occurrence of symptoms led to re-endoscopy in 11 patients. Re-ulceration was confirmed in six patients (33%), and mean time to ulcer recurrence was 18.2 weeks. Ulcer recurrence was treated with an increased dose of cimetidine and antacids. All the ulcers then healed again, and the patients remained well on a maintenance dose of cimetidine, 800 mg/day. None of the patients had to be operated on during the trial. Two patients developed gynaecomastia during maintenance treatment with 400 mg cimetidine a day. No serious untoward signs or symptoms occurred that necessitated withdrawal from the trial. It seems as if recurrent ulcers after proximal gastric vagotomy respond to cimetidine treatment approximately as do peptic ulcers in unoperated patients.

Adult↗
PubMed1981

Relapse of duodenal ulcer after treatment with trimipramine/antacids or cimetidine/antacids.

Ninety-three patients with duodenal ulcer were treated with trimipramine, 25 mg at night; cimetidine, 400 mg at night; or cimetidine, 1000 mg/day. In addition, all patients were given 20 ml antacids 1 and 3 h after meals. The healing rates after 6 weeks' treatment were 86%, 85%, and 100% in the three groups, respectively (differences not significant). After healing of the ulcers 88 of the patients were checked monthly during 1 year to study relapse rate. Endoscopy was performed on recurrence of symptoms suggesting relapse and after 6 and 12 months in all asymptomatic patients. Relapse was diagnosed in 64% of the patients in the trimipramine-treated group, in 48% in the 400 mg cimetidine group, and in 54% in th 1000 mg cimetidine group (differences not significant). The results suggest that ulcer recurrence is not commoner after treatment with standard dose of cimetidine than after a low dosage of cimetidine or trimipramine.

Antacids↗
PubMed1981

Adenylate cyclase activity in gastric mucosal biopsies and cAMP in gastric juice before and after cimetidine treatment in healthy subjects.

Previous studies have revealed augmented parietal call sensitivity to histamine stimulation after cessation of cimetidine treatment in healthy subjects. To elucidate one possible mechanism for this effect, we measured cAMP in gastric mucosa and gastric juice during histamine stimulation in vivo and histamine-stimulated adenylate cyclase activity in vitro in biopsy material obtained by gastroscopy. In eight healthy subjects the cAMP content of gastric corpus mucosal biopsies was measured before, during, and after infusion of 2.5 and 25.6 microgram . kg-1 . h-1 of histamine dihydrochloride. No increase in cAMP content was found. In 10 healthy subjects cAMP secretion into gastric juice was studied before and 36 to 84 h after cessation of 4 weeks' treatment with cimetidine, 1 g/day. No significant increase of cAMP output was found in response to infusion of 2.5 and 25.6 microgram . kg-1 . h-1 of histamine dihydrochloride either before or after the treatment period. Thus histamine does not stimulate cAMP secretion into gastric juice in man. In the same 10 subjects histamine-stimulated adenylate cyclase activity was studied in vitro in biopsy material obtained before and 60 h after cessation of cimetidine treatment. The dose-response curve of the adenylate cyclase activity was not shifted to the left. The results indicate that the augmented parietal cell sensitivity to histamine, seen after stopping cimetidine treatment in healthy subjects, is not due to increased sensitivity of the adenylate cyclase-cAMP system to histamine stimulation.

Adenylyl Cyclases↗
PubMed1981

The influence of hormones and drugs on gastric pepsin secretion. The role of vagal innervation.

Seven double-pouch dogs with one vagally innervated Amdrup pouch (AP) and one denervated and denervated mucosa at the same time in the same animal. Stimulation was done by food, a mixture of liver, heart and bonemeal, 10 g/kg. Cimetidine, 25, 50, 100, 200, and 400 mg; atropine, 0.031, 0.125, 0.5 and 1.0 mg; somatostatin, 0.5, 1.0, and 2.0 micrograms/kg/h; and secretin 2 U/kg/h, were given 60 min after the meal, one single dose on each day. Atropine and somatostatin lowered pepsin secretion in both pouches, significantly more in denervated mucosa for all doses of somatostatin and for the lower doses of atropine. Higher doses of atropine nearly abolished the secretion in both pouches. Cimetidine lowered pepsin output only in denervated mucosa. In innervated mucosa the output was unchanged or significantly increased (50 mg) by cimetidine. Secretin increased pepsin output significantly in both pouches, more in innervated mucosa. When the infusion of somatostatin was topped, a marked rebound effect was seen in the innervated pouch.

Animals↗
PubMed1981

Reduction of postprandial gastric acidity and pepsin concentration by ranitidine and antacids in healthy volunteers.

Small aliquots of gastric content were withdrawn every tenth minute for 7 h in 11 healthy volunteers with a maximal gastric acid output of more than 20 mmol h-1. After 20 min a steak meal was given. Ranitidine hydrochloride 100 mg administered with the meal increased postprandial gastric pH and reduced acid concentration markedly throughout the test. Two tablets of antacids with a neutralizing capacity of approximately 20 mmol per tablet 1 and 3 h after the meal reduced gastric acidity significantly less than ranitidine and did not prevent an increase in acidity to control level during the interval between the two doses. In the control experiments 40% of the pH readings during the 4 postprandial hours were at or above the pre-prandial pH levels. Antacids and ranitidine increased this to 85% and 96% respectively. Antacids had no effect after the fourth postprandial hour, had very little effect when given in addition to ranitidine, but reduced the mean four hour postprandial pepsin concentration more than ranitidine.

Administration, Oral↗
PubMed1981

Physiological stimulation of pepsin secretion. The role of vagal innervation.

The studies were performed on eight double-pouch dogs with one vagally innervated Amdrup pouch (AP) and one denervated Heidenhain pouch (HP), allowing comparison of pepsin secretion from innervated and denervated mucosa at the same time in the same animal. Food stimulation was done with a mixture of liver, heart, and bonemeal in doses of 1.25, 2.5, 5, 10, and 20 g/kg body weight, plus maximal stimulation by repeated meals of 5 g/kg every 15 min up to 10 times. 'Non-active' secretion of pepsin was determined by instillation in the pouches of 0.1 M and 0.005 M HCl dissolved in 0.15 M NaCl. The pepsin secretion in the HP equalled the 'non-active' output for all doses of food. In the innervated pouch there was an immediate, very high pepsin output similar to the response that can be elicited by 2-deoxy-D-glucose and bethanechol chloride. The secretion of pepsin was gradually reduced, but it was, as long as the volume and electrolyte secretion lasted. well above the 'non-active' level. The results show that stimulation of pepsin secretion by food is completely dependent on intact vagal innervation. The volume and acid output were increased as the dose of food was increased, but the concentration of pepsin was stepwise reduced when the volume increased, resulting in approximately the same output of pepsin for all doses of food. The pepsin to acid ratio was statistically higher in juice secreted from innervated than from denervated mucosa for all doses of food, for lower doses of histamine and pentagastrin, and for higher doses of bethanechol chloride.

Animals↗
PubMed1981

Augmented parietal cell sensitivity to histamine after cimetidine treatment in healthy subjects.

Basal and histamine-stimulated (0.4, 1.6, 6.4, and 25.6 micrograms . kg-1 h-1 of histamine dihydrochloride) gastric secretion was studied in 2 groups of 10 healthy young subjects before and 60 h after cessation of 4 weeks of cimetidine treatment, 1 g/day. Basal acid and pepsin outputs were not significantly different before and after treatment. After cessation of treatment acid output in response to the two lowest doses of histamine had increased significantly, whereas the output in response to the two highest doses of histamine was unchanged. The results are consistent with a hypersensitivity of the parietal cells to histamine stimulation after cessation of cimetidine treatment in healthy subjects. Pepsin output in response to histamine stimulation and catabolism of exogenous histamine were not influenced by treatment with cimetidine.

Adult↗
PubMed1980

The diuretic effect of secretin in man.

Six young healthy male students were studied with an intravenous infusion of 50 ml/h saline for three 2 h periods. In the second 2 h period pure natural secretin was added to the saline infusion in a dose of 2 CU/kg . h. Urine was collected separately in the three 2 h periods, and blood was drawn every 1 h. Urinary water, sodium, potassium, chloride, calcium, creatinine and solute excretion increased significantly during the 2-h secretin period. The clearance of sodium, potassium, chloride, calcium and solutes as a percentage of glomerular filtration rate (creatinine clearance) increased significantly, whereas tubular reabsorption of sodium as a percentage of filtrated sodium decrased significantly during secretin infusion. Even though plasma secretin remained elevated in the first half of the last 2 h control period, no diuretic effect was noted in this period. It would appear therefore that the diuretic effect of secretin most likely is a pharmagological effect only.

Body Water↗
PubMed1980

Inhibition of gastric secretion in man with a new H2-receptor antagonist, ranitidine.

Inhibition of pentagastrin-evoked gastric secretion of acid and pepsin by cimetidine and a new H2-receptor antagonist, ranitidine, was compared in nine healthy young subjects. On separate days cimetidine or ranitidine was administered by continuous intravenous infusions in graded doses. The results demonstrated that the inhibitory effect of ranitidine was 6 and 7.3 times as potent as cimetidine on a weight and a molar basis, respectively.

Cimetidine↗
PubMed1980

Effect of cimetidine treatment on parietal and chief cell sensitivity to histamine and on catabolism of histamine in duodenal ulcer patients.

Gastric acid and pepsin output in response to a low and a maximal dose of histamine was studied before and 60 h after cessation of 4 weeks of cimetidine treatment, 1 g/day, in 11 duodenal ulcer patients. Plasma histamine concentrations were measured in eight patients and the urinary excretion of intravenously injected 14C-histamine and its metabolites in two patients. Acid and pepsin output in response to the low dose of histamine as a percentage of the maximal response was on average 41.3% +/- 4.4% (S.E.M.) and 46.3% +/- 3.5% before treatment and 40.4% +/- 4.8% and 38.8% +/- 4.5% after cessation of treatment, respectively (p greater than 0.10). Thus, a course of treatment with cimetidine does not influence the sensitivity of the parietal and chief cells to histamine stimulation in duodenal ulcer patients. No significant change of plasma histamine concentrations and of catabolism of radiolabelled histamine was observed after cessation of cimetidine treatment.

Adult↗
PubMed1980

'Non-active' pepsin secretion compared with stimulated secretion by bethanechol, histamine, pentagastrin, and 2-deoxy-D-glucose. The role of vagal innervation.

The present studies were performed on a double-pouch dog with one vagally innervated Amdrup pouch (AP) and one denervated Heidenhain pouch (HP), allowing comparison of pepsin secretion from innervated and denervated mucosa at the same time in the same animal. 'Non-active' secretion of pepsin was determined by instillation in the pouches of 0.1 M and 0.005 M HCl, 0.15 M NaCl, and 0.03 M phosphate buffer, and well-known stimulators of gastric secretion such as histamine, pentagastrin, bethanechol, and 2-deoxy-D-glucose (2-DG) were tested as pepsigogues. Cholinergic stimulation by 2-DG and bethanechol (Urecholine) was clearly the most potent stimulus of pepsin secretion. 2-DG elicited secretion only from innervated mucosa, whereas the responses to bethanechol were similar in the two pouches. Histamine and pentagastrin were weak stimulators, but both provoked active and sustained secretion of pepsin when given in small doses. Higher doses of histamine strongly inhibited pepsin output. The effects of histamine were independent of vagal innervation. By contrast, the active stimulation by pentagastrin only took place in innervated mucosa. The highest outputs were seen in the lowest doses, but also very high doses of pentagastrin elicited active pepsin secretion in the AP. Medium doses of pentagastrin brought the secretion down the the 'non-active' level. The chief cells in the denervated mucosa were quite insensible to pentagastrin, and the pepsin output in the HP equalled the non-active' response at all dose levels.

Animals↗
PubMed1980

Treatment of duodenal ulcer with ranitidine, a new histamine H2-receptor antagonist.

Fifty patients with endoscopically verified duodenal ulcer were treated with either 100 mg of ranitidine hydrochloride (corresponding to 89.4 mg of ranitidine base) or identical placebo tablets twice daily under double-blind conditions. One patient did not attend for the second endoscopy and was excluded. Endoscopic examination after 4 weeks of treatment showed that the ulcer had healed in 23 out of 25 patients (92%) treated with ranitidine and in 11 out of 24 patients (46%) treated with placebo (P < 0.01). The ranitidine-treated patients had significantly less ulcer symptoms during treatment. Antacid consumption was also less in the ranitidine than in the placebo-treated group, but the difference was not significant. After 4 weeks in the double-blind study 14 of the 15 patients with unhealed ulcer received open treatment with ranitidine for 4-6 weeks. The ulcer healed in all but one patient. No serious side effects of ranitidine were observed.

Clinical Trials as Topic↗
PubMed1980

Treatment of duodenal ulcer with antacids in combination with trimipramine or cimetidine.

Ninetyfive patients with endoscopically verified duodenal ulcer were randomly allocated in a double blind manner to 3 different treatments. Thirtyfive patients were treated with trimipramine 25 mg nocte, 32 patients with cimetidine 400 mg nocte and 26 patients with cimetidine 200 mg 3 times a day and 400 mg nocte (standard dose). In addition all patients got intensive antacid treatment with LinkR, 20 ml 1 and 3 hours after meals. Two patients were excluded from the trial. After 6 weeks of treatment re-endoscopy revealed healed ulcer in 35 patients (86%) in the trimipramine group, in 32 patients (85%) in the group treated with low dose of cimetidine and in 26 patients (100%) in the group treated with standard dose of cimetidine. The differences in healing rate were not significant. The time until complete relief of pain was significantly longer in the trimipramine group than in the cimetidine groups. The drugs were well tolerated but constipation was reported by 31% of the patients.

Adult↗
PubMed1979

[Cimetidine].

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Cimetidine↗
PubMed1979

Thyrotrophin-releasing hormone inhibits the pentagastrin stimulated gastric secretion in man. A dose response study.

Actions of thyrotrophin-releasing hormone (TRH) have generally been confined to the central nervous system (CNS). We have studied the effect of increasing doses of TRH i.v. (8, 40, 200 and 1000 microgram/h) on pentagastrin-stimulated gastric secretion in ten normal individuals. All doses caused stepwise inhibition of gastric juice (volume), acid and pepsin output. When employing the largest dose of i.v. TRH (1000 microgram/h) the inhibition was 44% for gastric volume, 51% for acid output and 57% for pepsin output. This study shows that TRH inhibits gastric secretion, and indicates that TRH has actions outside the CNS in man.

Adult↗