PubMed Health⌕ Search

Biomedical subjects

B Kollberg

Publications and source records attributed to B Kollberg.

32 records · Page 2Linked to original sources
PubMed1981

Gastrointestinal protection by low-dose oral prostaglandin E2 in rheumatic diseases.

In a previous study oral prostaglandin E2 (PGE2) was shown to protect against indomethacin-induced gastrointestinal bleeding in patients with rheumatic diseases. This study examined whether a lower oral dose of PGE2, without acid antisecretory effect, is protective. Its methylated analogue 15(R)15 Me PGE2, which has effect on the acid secretion given orally, was also tested. Indomethacin, 50 mg three times daily, induced an increase in gastrointestinal bleeding measured by the 51Cr technique. PGE2, 033 mg three times daily, taken concomitantly significantly reduced fecal blood loss. 15(R)15 Me PGE2, 40 microgram three times daily, was also effective. The prostaglandins did not increase joint symptoms and had no significant side effects. It is suggested that the combination of nonsteroidal anti-inflammatory drugs with a low oral dose of E2 prostaglandins could be used clinically, especially in patients with rheumatic diseases.

Administration, Oral↗
PubMed1981

Acetazolamide interferes with the protective effect of prostaglandin E2 in the rat gastric mucosa.

Oral prostaglandin E2 protected the gastric mucosa against the damage induced by intraperitoneal indomethacin in the rat. Blocking of the gastric alkaline secretion by subcutaneous acetazolamide potentiated the ulcerogenic action of indomethacin and reduced or abolished the protective effect of a submaximal dose prostaglandin E2. The results are compatible with the hypothesis that stimulation of the alkaline secretion is one of the mechanisms by which prostaglandin E2 protects the gastric mucosa.

Acetazolamide↗
PubMed1981

Acute gastric erosions in the rat. I. Microangiography.

Microangiography of the gastric mucosa was performed in 16 adult rats 5 hours after administration of indomethacin. Superficial gastric erosions were induced irrespective of the route of administration. Microangiography demonstrated absence of vascular dilatation underneath the superficial gastric erosions, suggesting absence of protracted vascular spasm or microthrombosis in eroded areas. The presence of normal microangiographic appearances underneath the gastric erosions suggests that such lesions may be induced by mechanisms other than by vascular injury.

Angiography↗
PubMed1981

Acute gastric erosions in the rat. II. Viability of the gastric mucosa.

The autoradiographic appearance of the gastric mucosa, 5 hours after administration of indomethacin, was investigated in 29 adult rats. Indomethacin induced superficial gastric erosions. Autoradiography demonstrated the presence of viable gastric cells (as deduced by their ability to incorporate 3H-cytidine, an RNA precursor) not only in the mucosa without erosions, but also in the mucosa underneath the superficial erosions. The results indicate that indomethacin induced gastric erosions are not the superficial expression of the necrotic process taking place in the full thickness of the gastric mucosa at a particular site. A lumen-borne mechanism appears to be responsible for the formation of erosive areas in the mucosa.

Animals↗
PubMed1980

Effect of an H2-receptor blocking agent on diarrhoeas after extensive small bowel resection in Crohn's disease.

The effect of an H2-receptor blocking agent, cimetidine, on faecal losses of fluid, electrolytes and fat was examined in 10 patients with Crohn's disease, who had diarrhoeas after extensive small bowel resection. A randomized, double-blind and cross-over design was applied, and patients were hospitalized and on a defined diet during the study. Cimetidine, 4 x 400 mg, significantly reduced diarrhoeal volumes by an average of 22% (p less than 0.05) and faecal sodium by 27% (p less than 0.05). Patients with severe diarrhoeas responded better to treatment. No side-effects were recorded. The reported data suggest that cimetidine may be useful in symptomatic treatment of patients with severe diarrhoeas after extensive ileal resection. Due to deficient drug absorption, higher doses may be needed for optimal effect.

Adult↗
PubMed1980

Protective effect of prostaglandin E2 in the gastrointestinal tract during indomethacin treatment of rheumatic diseases.

Nonsteroidal antiinflammatory drugs (NSAID) induce the formation of bleeding gastric and intestinal ulcers in experimental animals. The damage can be prevented by prior local administration of prostaglandins, indicating that prostaglandins have protective properties on the gastrointestinal mucosa. The protective effect was studied in humans by measuring the fecal blood loss during indomethacin treatment of 18 patients with rheumatic diseases with and without concomitant oral supplementation with 1 mg prostaglandin E2 three times daily. The study had a randomized double-blind crossover design using 51Cr-labeled erythrocytes as marker of gastrointestinal bleeding. Indomethacin increased the daily fecal blood loss from 1.0 +/- 0.3 to 2.8 +/- 0.6 ml (P less than 0.005). When oral PGE2 was taken concomitantly, the blood loss was reduced to 1.1 +/- 0.2 ml daily (P less than 0.01), i.e., to the control level. Side effects of prostaglandin E2 were negligible, and the beneficial effect of indomethacin on joint status and symptoms was not interfered with. No changes were recorded in repeated blood tests except for a slightly reduced hemoglobin and a small but statistically significant reduction of serum-calcium during indomethacin treatment, an effect hitherto not described in normocalcemic human subjects. A protective effect on the gastrointestinal mucosa by oral prostaglandin E2 has by the present study been demonstrated also in humans. The protection is unrelated to the gastric acid secretion, which is not inhibited by oral prostaglandin E2. The finding may have clinical application, as gastrointestinal side effects and bleeding are common reasons for discontinuation of NSAID in patients with rheumatic diseases.

Adult↗
PubMed1979

The inhibitory effect of 15(R)15 methyl prostaglandin E2 and the interaction with atropine on stimulated gastric acid secretion in man.

The inhibitory effect of 15(R)15 methyl prostaglandin E2 (Me PGE2) on the gastric acid response to pentagastrin stimulation, 0.6 micrograms.kg-1.h-1, was examined in healthy male volunteers. Each subject underwent a control test and tests with intragastrically administered graded doses of 15(R)15 Me PGE2 as free acid (80, 140, 200, and 400 micrograms, n = 5) and as methylester (80, 140, and 200 micrograms, n = 6). The percentage inhibition of the acid output during 2 h after increasing doses of the free acid was 24 +/- 11, 49 +/- 7, 44+/-9, and 76 +/- 12%. Corresponding figures for the methylester were 35 +/- 2, 54 +/- 5, and 64 +/- 8%. Both volume and acidity were reduced. Side effects did not occur, except for moderate diarrhoea in one subject after 400 micrograms of the free acid. In a third series (n = 6) the combined effect of 80 micrograms methyl ester (44 +/- 5% inhibition) and 1.5 mg atropine sulphate was studied. Atropine alone gave a 43 +/- 6% inhibition by lowering the secreted volumes. For the combination the inhibition was 82 +/- 3%. Intragastric 15(R)15 Me PGE2 inhibited dose-dependently the pentagastrin-stimulated gastric acid response. Differences between the free acid and methyl ester of the analogue were not significant. Compared with other Me PGE2 compounds, 15(R)15 Me PGE2 was less effective per dose, but the dose range was broader and side effects were slight. Concomitantly given atropine had a significant additive inhibitory effect.

Adult↗