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Biomedical subjects

K F Hanssen

Publications and source records attributed to K F Hanssen.

At least 127 records · Page 7Linked to original sources
PubMed1978

Plasma prolactin in juvenile diabetics. 24-h studies with somatostatin.

In normal subjects during 24-hours saline infusion, plasma prolactin showed a number of small rises during day and night. The mean night-time level was significantly higher than the day-time level (8.2 +/- 0.6 ng/ml as against 4.7 +/- 0.5 ng/ml). In 12 insulin-dependent diabetics the 24 h plasma prolactin pattern was identical to that found in normals. Somatostatin infusion (4 mg/24 h in normals; 2--6 mg/24 h in diabetics) had no effect on the 24 h plasma prolactin pattern in either normals or in diabetics.

Adult↗
PubMed1978

A small dose of somatostatin inhibits the pentagastrin stimulated gastric secretion of acid, pepsin and intrinsic factor in man.

The effect of a small dose of somatostatin (0.05 mg/h) on the gastric secretion of acid, pepsin and Intrinsic Factor (IF) after stepwise increases in the dose of pentagastrin was examined in six healthy volunteers. The gastric secretion of acid, pepsin and IF in response to pentagastrin was significantly reduced by a continuous infusion of somatostatin. The pattern of inhibition indicates that somatostatin is a competitive inhibitor of pentagastrin in the stimulation of gastric secretion of both acid, pepsin and IF. This finding supports the hypothesis of a direct effect of somatostatin on the exocrine secretory cells of the stomach.

Blood Glucose↗
PubMed1978

Somatostatin inhibits gastric motility in response to distention.

Gastric motility and plasma gastrin concentration have been measured in 6 healthy volunteers before and after stepwise gastric distention. Distention was performed by filling a flaccid thin-walled bag, which was connected with a low pressure transducer for measuring intragastric pressure variations. Stepwise increase in gastric volume from 0-600 ml caused graded increases in gastric motility. No significant change was seen in the plasma gastrin level. When gastric distention was performed concomitantly with constant infusion of somatostatin (0.05 mg/h and 0.50 mg/h) in the same individuals on different days, motility was significantly reduced, without any changes in the plasma gastrin concentration. It is concluded that somatostatin, which probably plays a role in the gastro-intestinal tract, may have a physiological effect in the regulation of gastric motility too. This motility effect of somatostatin seems to be independent of any effect on the gastrin concentration.

Gastrins↗
PubMed1978

Actions of thyrotropin-releasing-hormone on gastrointestinal function in man. I. Inhibition of glucose and xylose absorption from the gut.

We studied serum glucose levels following a peroral glucose test in 6 healthy subjects on 2 alternate days in random order; with or without an i.v. TRH infusion for 3 hours (0.66 mg/hour). TRH infusion reduced serum glucose levels following oral glucose in all 6 subjects investigated. Serum insulin levels were reduced accordingly. Furthermore, serum xylose levels following peroral xylose were studied in the same 6 subjects. TRH infusion i.v. reduced serum xylose levels in all 6 subjects studied. I.v. glucose tolerance tests with or without an i.v. TRH infusion (0.66 mg/h) for 3 hours were studied in 4 healthy subjects. No change in serum glucose or insulin levels following TRH infusion was observed. We conclude that an i.v. infusion of TRH reduces serum levels of glucose following a peroral xylose load. TRH thus has marked actions on gastro-intestinal function in man inhibiting and/or retarding the absorption of glucose and xylose from the gut.

Adult↗
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

Increased serum prolactin in diabetic ketoacidosis; correlation between serum sodium and serum prolacting concentration.

In 8 patients with diabetic ketoacidosis, serum prolactin was measured and found to be elevated (24.8 +/- 10.2 ng/ml, mean +/- SEM). After correction of the ketoacidosis, the prolactin level decreased to 10.9 +/- 6.4 ng/ml (normal range men 4.9 +/-0.8, women 5.1 +/- 1.6 ng/ml). The scatter of prolactin values was wide. A study of the correlation between the serum prolactin values and chemical parameters that are altered in diabetic ketoacidosis was therefore undertaken. Serum prolactin values did not correlate well with the serum bicarbonate concentration or serum osmolality. However, a significant negative correlation between log serum prolactin concentration and serum sodium concentration was demonstrated (r = -0.61, P less than 0.01). It is suggested that serum prolactin may possible participate in sodium retention in man as has been demonstrated in studies on animals.

Adult↗
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↗
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↗
PubMed1974

Long-term infusion of growth hormone release inhibiting hormone in acromegaly: effects on pituitary and pancreatic hormones.

Growth hormone release inhibiting hormone (GH-RIH) was infused at a rate of 1.3 mug/min for 28 hours into four patients with acromegaly, two of whom also had clinical diabetes mellitus. Growth hormone and glucagon were suppressed throughout the infusion though delayed secretion of insulin occurred in association with both meals and an oral glucose load. Glucose tolerance was improved in one diabetic patient who was taking chlorpropamide while the other required much less insulin than usual. Secretion of endogenous thyroid-stimulating hormone was lowered in one euthyroid patient on carbimazole. Luteinizing hormone, follicle-stimulating hormone, ACTH, and prolactin were not affected. Serum somatomedin levels were reduced in one patient. There was a rapid rebound of all the suppressed hormones when the infusions stopped. Longer-acting analogues of GH-RIH will be needed before long-term therapy of acromegaly or diabetes mellitus becomes possible, but such preparations should be available soon for clinical trial.

Acromegaly↗