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Biomedical subjects

J Myren

Publications and source records attributed to J Myren.

At least 109 records · Page 6Linked to original sources
PubMed1977

Juxtapapillary duodenal diverticula and abnormalities by endoscopic retrograde cholangio-pancreatography (ERCP).

In a consecutive series of 174 patients the biliary and pancreatic ducts were demonstrated by endoscopic retrograde cholangio-pancreatography (ERCP). In 84 patients with normal duct systems, juxtapapillary diverticula were found in 5 patients (6%). In 90 cases with ductal abnormalities due to biliary concrements, dilated common bile duct and pancreatitis, diverticula were found in 35 patients (39%). In patients with abnormalities in both duct systems, diverticula were found in 52%, and in patients with changes in one duct system diverticula were found in 33%. The difference in occurrence of diverticula in patients with normal duct systems and pathological duct systems was statistically significant (p less than 0.02). The findings indicate a correlation between juxtapapillary diverticula and pathological changes due to biliary concrements, dilated common bile duct without concrements and pancreatitis.

Biliary Tract Diseases↗
PubMed1977

Inhibition of secretin release and pancreatic bicarbonate secretion by somatostatin infusion in man.

Five healthy students were investigated on two different days with or without a constant infusion of somatostatin (500 microgram/h) into an arm vein a fluoroscopically placed Lagerlöf tube was used for the collection of gastric and duodenal juice. After 30-min basal period, 40 ml 100 mmol/l HCl was infused into the midpart of the duodenum over 5 min through a thin catheter attached to the tube. Plasma immunoreactive secretin was measured by radioimmunoassay employing 125I-labelled synthetic secretin, antibody against synthetic secretin, and standards prepared from pure natural porcine secretin. Secretin levels without somatostatin infusion were 4.6+/-0.7 pmol/l (mean+/-S.E.M.) basally and rose to a peak of 21.8+/-6.2 pmol/l after duodenal acidification (p less than 0.05) and with somatostatin infusion were 4.4+/-0.4 pmol/l basally and rose to a peak of 6.7+/-1.7 pmol/l (n.s.) after duodenal acidification. Pancreatic bicarbonate output increased from 8.0+/-2.5 mumol/min (mean+/-S.E.M.) to 283+/-44 mumol/min without somatostatin infusion (p less than 0.05) and from 6.7+/-2.1 mumol/min to 70+/-13 mumol/min somatostatin (p less than 0.05). This study shows that somatostatin (500 microgram/h can inhibit the release of secretin and the pancreatic bicarbonate secretion after duodenal acidification in man.

Adult↗
PubMed1977

The effect of somatostatin on pentagastrin-stimulated gastric secretion and on plasma gastrin in man.

Three experiments were carried out in each of 6 healthy students on separate days, in a randomized order. Intravenous saline infusions were given for one hour basally in each experiment. During the second hour either pentagastrin, pentagastrin and somatostatin, or somatostatin alone were given. Gastric juice was collected continuously during all experiments. Somatostatin decreased the volume of gastric secretion and the concentrations of acid and pepsin, and output of acid, pepsin, and intrinsic factor (IF). The plasma gastrin concentration was not changed by somatostatin. A rebound effect was seen on pepsin and IF outputs after cessation of somatostatin, and on blood sugar concentration. The present study suggests that somatostatin acts on gastric secretion either directly or by mechanisms other than by inhibition of gastrin. The rebound of pepsin and IF indicates a release-inhibiting action on these substances similar to the effect of somatostatin on the release of some hormones.

Blood Glucose↗
PubMed1977

Plasma gastrin and gastric secretory response to duodenal perfusion with liver extract in healthy human subjects.

The stomachs of 8 healthy volunteers were intubated with a Levine tube under radiological control. In addition, a thin polyethylene tube was placed in the proximal duodenum. After a 1-hour period with no perfusion, the duodenum was perfused for two hours with 15% liver extract (LE) (pH 4.5--5.5; 1027 mosm/kg water) at a rate of 100 ml/hour either alone or in combination with intravenous infusion of different doses of exogenous pentagastrin. All subjects were also tested with the tubes in place for 3 hours, but with no perfusion or pentagastrin. Reflux to the stomach was monitored by addition of radioactive B12 to the perfusates. Plasma gastrin, gastric acid, and pepsin were measured in 15-minute periods. During perfusion of the proximal duodenum, where reflux of the perfusates was less than 4%, only a slight and inconstant change in plasma gastrin was seen. Gastric acid and pepsin outputs were increased to approx. 18% and 25% of the maximal pentagastrin stimulation respectively. Whereas 15% LE was shown to release gastrin by antral perfusion however, such release was not found by duodenal perfusion, except where reflux to the antrum was seen. The results suggest that intestinal stimulation of gastric secretion exists, but has not been found to be gastrin dependent in the present investigation.

Duodenum↗
PubMed1976

Routine and blind histological diagnoses on colonoscopic biopsies compared to clinical-colonoscopic observations in patients without and with colitis.

Of the 110 patients examined, complete agreement was found between the blind and routine histological studies in the sections from 69 patients (63%), between the blind histological study and that of colonoscopy in 66 patients (60%), and between the routine histological diagnoses and those of colonoscopy in 73 patients (66%). The diagnosis of a normal colonic mucosa was made by blind study on colonoscopic biopsies in 32 patients, by the routine one in 36 patients, and by clinical-colonoscopic examination in 40 cases, the percentage of agreement with the colonoscopic diagnosis being 68 and 72, respectively. The diagnosis of unspecific non-ulcerative colitis was made by the blind histological study in 43 patients, by the routine histological examination in 58 cases, and by colonoscopy in 41 patients. The percentage of agreement between the histological studies and the clinical-colonoscopic diagnoses was 61 and 78, respectively. A diagnosis of ulcerative colitis was made by the blind histological study in 35 patients, by the routine histological examination in 16, and by colonoscopy in 27 cases. The percentages of agreement between the histological studies and the diagnoses by clinical-colonoscopic examination were 82 and 59, respectively. The differences in symptomatology between groups were small, except for a high occurrence of diarrhoea and blood in stool in ceses with ulcerative colitis, as evaluated by blind histological study. The findings stress the importance of following defined criteria for histological examination.

Biopsy↗
PubMed1976

The diagnosis of colitis by colonoscopy with biopsy and X-ray examination. A blind comparative study.

The examinations were performed in 40 outpatients, of whom 21 were women. From the rectal and colonic mucosa 185 biopsies were obtained. The X-ray examination was performed within one week from the colonoscopy, using a conventional barium enema. A complete agreement between the colonoscopic diagnosis and that of the directed biopsy was found in 33 cases (80 per cent), and minor disagreements in 3 cases. A complete agreement between the colonoscopic and X-ray diagnoses was obtained in 22 patients (55 per cent), and minor disagreements in 16 cases, most of whom showed "unspecific" non-ulcerative colitis. In 3 cases with ulcerative colitis a normal colon was found by X-ray. A higher percentage of cases showed decreased haustration by X-ray examination than by colonoscopy, whereas a fairly equal percentage of ulceration was detected by the two methods. Erosions, mucus covering, oedema, vascular injection, and bleedings were not detected by X-ray examination.

Adult↗
PubMed1976

Gastric secretory response to different doses of carbachol and pentagastrin in man.

In 6 healthy students, the gastric secretion of acid, pepsin, and IF was measured during one hour at basal conditions, and during one hour of stimulation with 0.01 mug/kg/h and thereafter during one hour of stimulation with 0.1 mug/kg/h of pentagastrin. On separate days the same dose of pentagastrin was given in combination with 0.15 mug/kg/h or 1.5 mug/kg/h of carbachol, or stimulation was performed with each of the two doses of carbachol alone. A dose-dependent relationship was found between carbachol and the output of acid, pepsin, and IF. The responses to carbachol were independent of changes in plasma gastrin concentration. The acid- and IF-secretions stimulated by the largest dose of pentagastrin were significantly increased by the largest dose of carbachol, whereas the secretion of pepsin was not. Pentagastrin and carbachol seem to interact by competitive augmentation on the gastric secretion of acid and IF.

Adult↗
PubMed1976

Somatostatin inhibits insulin-stimulated gastrin release and gastric secretion of acid, pepsin, and intrinsic factor (IF) in duodenal ulcer patients.

The effect os somatostatin (0.6 mg/hour) on insulin-stimulated gastrin release and gastric secretion of acid, pepsin, and IF has been examined in 6 unoperated patients with duodenal ulcer. Gastrin release and gastric secretion of acid, pepsin, and IF in response to insulin alone (0.15 IU/kg bw. iv.) were significantly reduced by simultaneous administration of somatostatin. This finding indicates an inhibitory effect of somatostatin on insulin-induced gastrin release and gastrin secretion in addition to the already known effects of somatostatin.

Blood Glucose↗