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Biomedical subjects

C Johansson

Publications and source records attributed to C Johansson.

At least 325 records · Page 18Linked to original sources

Effects of graded doses of somatostatin on gallbladder emptying and pancreatic enzyme output after oral glucose in man.

Effects of intravenous somatostatin on the secretion, motility and absorption in the upper gastrointestinal tract after 75 g oral glucose were examined in healthy subjects with a quantitative multiple indicator dilution method. This report deals with the effects on the gallbladder emptying and the pancreatic enzyme output. Intake of a hypertonic glucose solution induces rapid gallbladder emptying. After early peaks, both biliary and pancreatic enzyme outputs remain at a steady lower level to the end. Somatostatin, started 20 min before the oral load, inhibited dose-dependently the gallbladder emptying and pancreatic enzyme secretion. A maximal inhibition was attained by 1.5 microgram . min-1, and 0.05 microgram . min-1 somatostatin gave a significant 40% reduction. The inhibition persisted in the postinfusion period and was followed by delayed rebound outputs. The gallbladder emptying was completely arrested for variable periods of time, but the pancreatic enzyme secretion was never totally blocked. The promptly established arrest of the gallbladder differed from the slowly initiated inhibition of the gastric and intestinal propulsion. It is proposed that the multiple ways of action of somatostatin and different stimulatory levels contribute to the discrepancies. The study shows that somatostatin induces dose-dependent, long-lasting inhibitions of the biliary and pancreatic responses to oral glucose. The minimal effective dose was a hundred times lower than the dose tested in previous studies in man.

Administration, Oral↗

Serum level of biliary glycoprotein I, a determinant of cholestasis, of similar use as gamma-glutamyltranspeptidase.

Biliary glycoprotein I (BGP I), a constituent of normal bile and serum, is a glycoprotein (mol. wt. approximately 90,000) containing about 40% carbohydrate. Serum BGP I (S-BGP I) was determined by means of a double-antibody radioimmunoassay in patients with liver and gastrointestinal disease and in healthy individuals. The serum levels of five liver enzymes (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase (S-ALP), gamma-glutamyltranspeptidase (S-GT), and lactic dehydrogenase), bilirubin (total and conjugated), and bile acids (cholic and chenodeoxycholic acid) were determined in parallel. Healthy individuals had 0.5 +/- 0.3 mg/l of S-BGP I (mean +/- 2 S.D.; range, 0.2-0.9 mg/l). Most patients with liver disease (chronic hepatitis, alcoholic cirrhosis, primary biliary cirrhosis) had elevated levels, up to 5-10 times the upper reference limit, whereas most patients with gastrointestinal disease (ulcerative colitis, Crohn's disease, other GI diseases) had normal values. In patients with liver disease S-BGP I was positively correlated (p less than 0.0005) to S-GT. In primary biliary cirrhosis a positive correlation (p less than 0.005) between S-BGP I and S-ALP was also obtained. All other comparisons between S-BGP I and the other liver function tests showed non-significant correlations. It is concluded that S-BGP I is a determinant of cholestasis of similar use as S-GT.

Adolescent↗

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↗

Evaluation of fasting serum bile acid concentration in patients with liver and gastrointestinal disorders.

Fasting concentrations of S-cholate, S-chenodeoxycholate, S-aminotransferases, S-bilirubin, S-alkaline phosphatases, and S-glutamyltransferase were determined in 564 outpatients with disorders of the liver and gastrointestinal tract. Unsulphated conjugates of cholic (fS-C) and chenodeoxycholic acid (fS-CDC) were determined by radioimmunoassay. In patients with increased serum bile acid concentrations fS-C and fS-CDC were linearly correlated, and the fS-C/fS-CDC ratio was similar in all patient groups. The incidence of false-positive results of fS-CDC was probably due to inadequate fasting and comparison of fS-C only with the liver tests. In 51 patients with verified cirrhosis fS-C was significantly correlated with S-bilirubin in a semilogarithmic relation but not with S-alkaline phosphatases or S-glutamyltransferase. fS-C was found to be a sensitive indicator of liver disease in the anicteric stage. Of 207 patients with inflammatory bowel disease, 63 had 1 or several of the results of liver tests for cholestasis elevated. There was no correlation between the different tests. In these patients and all patients with gastrointestinal disorders the commonest single finding was an elevation of S-alkaline phosphatases not associated with cholestasis.

Bile Acids and Salts↗

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↗

Endoscopic YAG-laser treatment in massive upper gastrointestinal bleeding. Report of a controlled randomized study.

In patients with massive upper gastrointestinal bleeding the results of endoscopic control by coagulation with YAG-laser have been compared with the results of an active surgical approach with early operation in a controlled randomized study. The laser coagulation was done at admission in patients in whom an actively bleeding lesion was diagnosed at endoscopy. Of the 66 patients belonging to the laser group, 23 were bleeding at admission and endoscopy, and in 15 of these coagulation was attempted and initial haemostasis was achieved in 14. Seven of the latter rebled and five of them were then operated upon with on postoperative death. Two patients died from bleeding oesophageal varices and hepatic failure. In the patient in whom haemostasis was not achieved, an operation was done for a duodenal ulcer. She died postoperatively. Of the 43 patients belonging to the laser group and not bleeding at endoscopy, nine patients rebled and three of them were operated upon, the with on postoperative death. An additional four patients died in this group, three of bleeding oesophageal varices in combination with hepatic failure and one of bleeding from an unknown source. Sixty-nine patients belonged to the control group and in 19 of these patients bleeding lesions were diagnosed at endoscopy. Five of these were operated upon, with two postoperative deaths. An additional three patients died of bleeding oesophageal varices and hepatic failure. Of the 50 patients belonging to the control group and not bleeding at endoscopy, eight later showed signs of recurrent bleeding. Four of them had oesophageal varices and two died. The other four with recurrent bleeding were operated upon with no postoperative mortality. Thus nine patients (five with oesophageal varices) died in the laser group and seven (five with oesophageal varices) in the control group. There was no statistically significant difference between the two groups regarding mortality, need of blood transfusion or time of treatment in the hospital. However, the material is too small to make any definite conclusions, and further studies are necessary in which laser treatment is compared with an aggressive surgical policy with early operations.

Aged↗

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↗

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↗

Release of gastrin and somatostatin into the gastric lumen of healthy subjects and patients with duodenal ulcer and achlorhydria.

Gastrin and somatostatin were measured in alkaline gastric instillates in normal subjects, patients with duodenal ulcer disease in quiescent state and in patients with achlorhydria. Both peptides were released into the lumen. The gastrin-somatostatin ratio (G/S) in healthy subjects was approximately three. Duodenal ulcer patients had significantly lower G/S ratio due to lower gastrin and higher somatostatin levels whereas in patients with achlorhydria, the G/S ratio did not differ from normal subjects.

Achlorhydria↗

Decreased release of somatostatin into the portal vein following electrical vagal stimulation in the cat.

Electrical vagal stimulations were performed in anesthetized cats, in which the spleen and the intestine below the duodenum had been removed. The cats were provided with acute antral pouches which were perfused during the experiments. Insulin, glucagon, gastrin and somatostatin were measured in portal vein blood (consisting of blood from the stomach and the pancreas). The antral perfusates were analyzed for gastrin and somatostatin. Electrical vagal stimulation increased the release of insulin and glucagon into the portal vein. Gastrin was elevated in antral perfusates and portal vein blood, whereas somatostatin increased the antral perfusates, but was reduced in portal vein blood. We assume that antral somatotostatin, like gastrin, is released into the blood. The finding that portal vein somatostatin was decreased following vagal stimulation, indicates that the release of somatostatin from another large source of somatostatin, presumably the fundic region of the stomach or the pancreas, was decreased by vagal activation.

Animals↗

Output of bile and pancreatic enzymes after test meals with different fat content. Influence of body weight on pancreatic enzyme composition.

The output of bile and pancreatic enzymes after two mixed meals with different fat content was studied in 16 healthy volunteers of normal body-weight. A quantitative multiple indicator dilution method was used. The delivery of more fat per time to the duodenum after the fat rich compared to the low fat meal was followed by the emptying of more bile but did not significantly increase the pancreatic response. The ratio between amylase and lipase was constant throughout the course of a single experiment but differed between the subjects. The ratio decreased with an increasing body weight, indicating a relative dominance of amylase over lipase in the lighter and the reverse in the heavy subjects. The same correlation was found when results from a previously reported series with a glucose containing mixed meal were reexamined. It is proposed that long time dietary differences might influence the enzyme composition of the postprandial pancreatic secretion.

Adult↗

Effect of intraluminal pH on the release of somatostatin and gastrin into antral, bulbar and ileal pouches of conscious dogs.

Experiments were performed on conscious dogs with chronic pouches of the antrum, the duodenal bulb or the ileum, which were perfused with solutions of varying pH. Gastrin and somatostatin levels were measured in the perfusates. When the pouches were perfused with 0.15 M NaCl only small amounts of gastrin and somatostatin (1 pmol/min) were released into the lumen of the antrum and of the duodenal bulb. By lowering pH of the perfusion fluid a pH dependent release of somatostatin was induced into the lumen of the antrum and the duodenal bulb. Perfusion with 0.1 M HCl caused a large output of somatostatin (6--60 pmol/min) into the pouches. The upper pH limit for stimulation of the intraantral or intrabulbar somatostatin release appeared to be approximately pH 3--4. Somatostatin was also released into ileal perfusates at intraluminal pHs below 3--4. Lowering of pH in the antral pouches caused an increased intraluminal gastrin release, which was quantitatively less impressive than that of somatostatin. Occasionally also the gastrin release into the duodenal bulb increased during perfusion with 0.1 M HCl, whereas no such release was induced by acidification of the lumen of the ileum. It is suggested that the inhibition of gastrin release observed at low intraantral pH is mediated by a local effect of somatostatin, since this peptide is released in a pH dependent manner in the antropyloric region. It is also suggested that acidification of any region of the gastrointestinal tract will stimulate the release of peptides from all endocrine cells of the open type, probably by an unspecific effect on the membrane. Thus both gastrin and somatostatin are released by acidification of the antrum, but in the presence of high local levels of somatostatin, the release of gastrin is substantially inhibited.

Animals↗

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↗

Helix pomatia a hemagglutinin, a surface marker for bovine T-lymphocytes.

Bovine peripheral blood lymphocytes (PBL) were isolated from blood collected from 6 cattle. After treatment with neuraminidase, 40 or 60% of the cells were shown to combine with Helix Pomatia A hemagglutinin (HP) depending whether a direct or indirect fluorescence technique was used. About 20% of the cells were Ig-bearing. With double staining fluorescence technique, it was shown that cells attaching to HP were not Ig-bearing and the reverse. With the aid of HP, covalently bound to Sepharose, Ig-bearing cells could be separated from cell populations attaching to HP. The fraction of cells forming rosettes with sheep erythrocytes was proportional to that of HP attaching cells both before and after fractionation on the HP column. It is therefore concluded that HP is a marker for bovine T-cells, and that this lectin may be used to separate B-cells from T-cells.

Animals↗