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Biomedical subjects

A Berstad

Publications and source records attributed to A Berstad.

At least 235 records · Page 13Linked to original sources
PubMed1979

Actions of thyrotropin-releasing hormone on the gastrointestinal function in man. II. Inhibition of pentagastrin-stimulated acid secretion.

The pentagastrin-stimulated gastric volume and acid output were measured with and without an i.v. thyrotropin-releasing hormone (TRH) infusion (666 microgram/h). TRH inhibited the pentagastrin (6 microgram/kg s.c.) stimulated volume to 67.5 +/- 8.4% (p less than 0.01) and the acid output to 65 +/- 8.4% of control infusion values (mean +/- S.E.M.). It is concluded that TRH inhibits the pentagastrin-stimulated gastric secretion in man.

Adult↗
PubMed1979

Parietal and chief cell sensitivity to pentagastrin stimulation before and after cimetidine treatment for duodenal ulcer.

Gastric acid and pepsin output in response to 0.10 and 6.0 microgram . kg-1h-1 of pentagastrin was studied in ten duodenal ulcer patients before and after cessation of 6 weeks of cimetidine treatment, 1 g/day. Acid output in response to the low dose of pentagastrin was on average 63% of the response to the high dose before and on average 65% after treatment. The corresponding values for pepsin output were on average 88% both before and after treatment. Thus, the parietal and chief cell sensitivity stayed unchanged after cimetidine treatment. Mean maximal acid output decreased insignificantly, from 39.4 mmol/h before 34.9 mmol/h after cimetidine treatment. The results suggest an unchanged gastric acid and pepsin secretion capacity after short-term treatment with cimetidine for duodenal ulcer.

Cimetidine↗
PubMed1979

Effect of cimetidine on histamine- and pentagastrin-stimulated gastric secretion in healthy subjects.

Cimetidine-induced inhibition of gastric acid and pepsin secretion in response to histamine and pentagastrin simulation was studied in four healthy young subjects. Different doses of histamine and pentagastrin were administered alone and in combination with cimetidine on separate days; the order of administration was randomized. As the dose of histamine increased, the inhibitory effect of 0.6mg.kg-1h-1 of cimetidine on acid output decreased. With supramaximal histamine stimulation the inhibition was completely overcome. These results are consistent with competitive inhibition of histamine-stimulated acid output by cimetidine in man. After pentagastrin stimulation inhibition of acid output by cimetidine could not be overcome by increasing the dose of the stimulant, suggesting a noncompetitive inhibition of pentagastrin-evoked acid output. It is concluded that the kinetics of cimetidine-induced inhibition of histamine- and pentastrin-stimulated gastric acid output are different. At approximately half maximal stimulation of acid secretion, cimetidine was a more potent inhibitor of histamine than of pentagastrin. Pepsin output in response to both histamine and pentagastrin stimulation was also inhibited by cimetidine.

Adult↗
PubMed1979

Maintenance treatment of duodenal ulcer patients with a single bedtime dose of cimetidine.

Fifty-eight patients with endoscopically verified duodenal ulcers were treated with cimetidine, 1 g/day, for 6--10 weeks. The ulcers healed in 52 out of the 54 patients completing the treatment (96.3%). Forty-seven of the patients with healed ulcer were randomly allocated to 1 year of maintenance treatment, 23 patients with cimetidine, 400 mg at night, and 24 patients with placebo tablets. In the cimetidine-treated group 2 out of the 20 patients (10%) completing the trial had recurrence of ulceration, whereas 16 out of the 23 patients (70%) completing the placebo treatment had ulcer recurrence (p less than 0.001). The drug was well tolerated and, except for a marked increase in serum transaminases in three patients, no serious side effects were seen.

Adult↗
PubMed1979

Parietal and chief cell sensitivity to histamine and pentagastrin stimulation before and after cimetidine treatment in healthy subjects.

Gastric acid and pepsin output in response to 2.5 and 25.6 micrograms . kg-1h-1 of histamine dihydrochloride and 0.10 and 6.0 micrograms . kg-1h-1 of pentagastrin was studied before and after cessation of 4 weeks of cimetidine treatment, 1 g/day, in 10 healthy volunteers. Acid output in response to the low dose of histamine increased significantly from an average of 6.7 mmol +/- 1.3 mmol (S.E.M.) before to 10.1 mmol +/- 0.9 mmol after treatment (p = 0.02), whereas acid output in response to the maximal dose of histamine was not significantly different. Parietal cell sensitivity to histamine stimulation increased significantly after the treatment period from a mean of 28.2% +/- 3.2% before treatment to 49.3% +/- 2.8% afterwards (p less than 0.01). The results indicate augmented parietal cell sensitivity in response to histamine stimulation after withdrawal of cimetidine. Both acid output in response to the two doses of pentagastrin and parietal cell sensitivity to pentagastrin stimulation were not significantly different after cessation of cimetidine treatment. Pepsin output and chief cell sensitivity to histamine and pentagastrin stimulation were not significantly influenced by cimetidine treatment.

Cimetidine↗
PubMed1978

Effect of cimetidine on pentagastrin-stimulated gastric acid and pepsin secretion before and after 6 weeks of cimetidine treatment.

To see whether the effect of cimetidine changes during a treatment period, the effect of intravenous cimetidine on pentagastrin-stimulated gastric acid and pepsin secretion was studied before and after a 6-week course of oral cimetidine treatment, 1 g/day, in 10 duodenal ulcer patients. Pentagastrin, 1.5 microgram . kg-1 . h-1, was infused for 165 min, and cimetidine, 1.2 mg . kg-1 . h-1, was added by concomitant infusion during the last 90 min. The second secretion test was carried out 60 hours after the last dose of cimetidine. Acid and pepsin secretion, in response to pentagastrin stimulation, was not significantly changed after 6 weeks of daily cimetidine treatment. The response to pentagastrin plus cimetidine was, however, significantly higher at the end than at the start of the treatment period. The results suggested a slightly reduced effect of cimetidine after prolonged use.

Adult↗
PubMed1978

Effect of cimetidine on pentagastrin-stimulated gastric secretion before and after proximal gastric vagotomy for duodenal ulcer.

Nine patients with duodenal ulcer were studied before and 2--3 months after proximal gastric vagotomy (PGV). Infustion or cimetidine, 1.2 mg.kg-1h-1, reduced mean gastric acid output, in response to infusion of 1.5 microgram.kg-1h-1 of pentagastrin, by, on an average, 79.4% before and 79.1% after vagotomy. The corresponding values for pepsin output were 66.5% before and 77.0% after the operation. The values were not statistically different. Thus, in terms of per cent inhibition, cimetidine was similarly effective before and after PGV. No correlation was found between per cent reduction of acic output by vagotomy and by cimetidine. The effect of the drug was added to that of the vagotomy. Patients with relapse ulcer after vagotomy are therefore interesting candidates for cimetidine treatment.

Cimetidine↗
PubMed1978

The effect on intestinal calcium absorption of somatostatin in man.

Somatostatin has been detected in the gastrointestinal tract and has been shown to have wide actions on gastrointestinal function. Using an isotope method with 51Cr as a stool marker, we have examined the absorption of 47Ca in 9 healthy volunteers with and without infusion of cyclic somatostatin (250 microgram/h for 2 hours). Both serum and faecal measurements show reduced 47Ca-absorption during somatostatin infusion, net absorption falling from 53.0 +/- 14% without to 40.4 +/- 13% with somatostatin. Possible explanations are discussed with special emphasis on the possibility of an inhibition of active calcium transport, which may be a more general mode of somatostatin action.

Calcium↗
PubMed1977

Gastric mucosal damage caused by plain and microencapsulated acetylsalicylic acid tablets in healthy subjects: a gastrocamera study.

In a randomized, cross-over study plain acetylsalicylic acid (ASA) tablet and microencapsulated ASA tablets were given in doses of 1 gram 3 times a day for 3 days to 8 healthy subjects with no previous gastrointestinal disturbances. Gastrocamera examinations were performed before the ASA treatment and 1--2 hours after the last dose of ASA. The gastric mucosa appeared macroscopically normal at all the control examinations; whereas musocal bleeding was evident in all the subjects after the ASA treatment. There was no statistically significant difference between the plain ASA and the microencapsulated ASA preparations. No correlation could be found between the ASA concentration in plasma and the gastric mucosal damage.

Adult↗
PubMed1977

Effect of cimetidine on pentagastrin-stimulated gastric secretion in healthy man.

Two series of experiments were carried out in three healthy volunteers. In one series increasing doses of cimetidine were tested on a constant background stimulation with 0.15 microgram-kg-1h-1 of pentagastrin. In the other series of experiments increasing doses of pentagastrin were given either alone or in combination with a fixed dose of cimetidine (1.2 mg-kg-1h-1). Pentagastrin and cimetidine were given as continuous intravenous infusions, the various doses tested on separate days. The inhibition of acid output in response to pentagastrin stimulation increased almost linearly with the log dose of cimetidine. Fifty per cent inhibition of the response to 0.15 microgram-kg-1h-1 of pentagastrin was achieved by about 0.6 mg-kg-1h-1 of cimetidine. 2.4 mg-kg-1h-1 of cimetidine gave on average 90% inhibition. The inhibition caused by cimetidine decreased to a minimum of 57% and could not be overcome by increasing the doses of pentagastrin. The results suggest a mixture of competitive and noncompetitive interaction. The effect of cimetidine on pepsin secretion was less regular. Generally, pepsin output was less inhibited than acid output.

Adult↗
PubMed1976

[Fat in feces].

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Feces↗