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Biomedical subjects

M K Müller

Publications and source records attributed to M K Müller.

69 records · Page 4Linked to original sources
PubMed1988

Differential sensitivity of rat exocrine and endocrine pancreas to cyclosporine.

The effect of 5, 10, and 20 mg/kg bw cyclosporine on rat endocrine and exocrine pancreatic function was studied. Glucose-dependent insulin secretion from the endocrine pancreas was shown to be significantly impaired 8 days after cyclosporine was given once daily at a dose as low as 5 mg/kg. CCK-8-stimulated amylase and lipase secretion were less sensitive to the noxious effect of cyclosporine being impaired at a dose of 10 mg/kg. Trypsin secretion was shown to be impaired at 20 mg/kg cyclosporine only. Our results demonstrate that cyclosporine causes dose-dependent impairment of both pancreatic endocrine and exocrine functions: the endocrine pancreas being more sensitive to the noxious action than the exocrine pancreas.

Amylases↗
PubMed1988

Prevention of toxic effects of cyclosporin on pancreatic B-cells of rats by Rioprostil, a new prostaglandin analogue.

Cyclosporin 5, 10, and 20 mg/kg bw was given to rats once daily intragastrically and caused a dose dependent, significant decrease of glucose dependent insulin release from the arterially perfused isolated pancreas, without affecting animal behaviour, weight gain, microscopic appearances of the pancreas, or kidney function. Subcutaneous injection of a new synthetic prostaglandin analogue Rioprostil 7.5 micrograms/kg bw twice daily completely prevented the effect of cyclosporin 5 mg/kg bw and protected significantly against the effects of cyclosporin 10 and 20 mg/kg bw.

Animals↗
PubMed1988

[Treatment of chronic non-secretory diarrhea in ileostomy with the long-acting somatostatin analog SMS 201-995].

A patient with chronic refractory non-secretory diarrhea following ileostomy was treated with the long acting somatostatin analogue SMS 201-995. Under treatment with somatostatin stool weights were drastically reduced and electrolyte dysbalance was normalized within a few days. This case report shows that somatostatin is also therapeutically effective in non-secretory diarrhea.

Colectomy↗
PubMed1987

[Tumor lysis syndrome in a young patient with Burkitt-type lymphoblastic lymphoma].

A tumor lysis syndrome with hyperkalaemia, hyperphosphataemia, hyperuricaemia and hypocalcaemia developed 48 hours after start of combined cytostatic treatment in a 16-year-old boy with Burkitt's lymphoma. Despite prophylactic administration of allopurinol and urinary alkalization, postrenal precipitation of urates and calcium phosphate caused acute renal failure. Ureteric splinting and percutaneous fistulization of the contralateral renal pelvis became necessary. Elevated renal retention values became normal after these measures and infusions with balanced alkalized electrolyte solutions, and the hypocalcaemia was counteracted.

Adolescent↗
PubMed1986

Effect of GIP on insulin release to intravenous glucose infusion in hyperthyroid rats.

Triiodothyronine induced hyperthyroidism caused significantly elevated basal and stimulated glucose and insulin levels in rats. The release of Gastric Inhibitory Polypeptide (GIP) following an oral glucose load was not significantly different between euthyroid and hyperthyroid rats. The insulin response, however, was significantly higher in hyperthyroid rats. Following intravenous glucose hyperthyroid rats showed a diminished insulin response when compared with euthyroid rats but intravenous infusion of glucose together with GIP caused a significantly higher insulin response in hyperthyroid rats. It is hypothesized that in hyperthyroidism there is an increased sensitivity to the insulinotropic action of GIP and that this mechanism could emphasize the importance of the enteroinsular axis in pathophysiological states.

Administration, Oral↗
PubMed1986

Increased release of gastrin in hyperthyroid rats in vitro.

The extrinsically denervated and vascularly perfused stomach of the hyperthyroid rat exhibits an increased basal gastrin release and an exaggerated response to stimulation with the b-agonist isoproterenol. The b-blocker propranolol does not inhibit the increased basal release of gastrin, but completely blocks the effect of isoproterenol. Vagal stimulation is not different between hyperthyroid and euthyroid rats. We conclude, that there are two mechanisms which are responsible for the increased release of gastrin in hyperthyroidism: firstly a direct effect of thyroid hormones on gastrin cells, and secondly an increase in sensitivity of gastrin cells towards b-adrenergic stimulation.

Animals↗
PubMed1986

Interaction of acetylcholine and gastric inhibitory polypeptide on endocrine and exocrine rat pancreatic secretion: augmentation of acetylcholine-induced amylase and volume secretion by the insulinotropic action of gastric inhibitory polypeptide.

Exocrine pancreatic secretion is under partial control of endocrine pancreatic hormones. We studied the interaction of three doses of acetylcholine (Ach), a stimulator of exocrine and endocrine pancreatic secretion, with one dose of gastric inhibitory polypeptide (GIP) which is strongly insulinotropic, but has no effect on exocrine pancreatic secretion. The effects of Ach and GIP on insulin secretion from the rat pancreas were additive at 0.05 X 10(-6) M Ach and slightly, but not significantly less than additive at 0.25 or 2.5 X 10(-6) M Ach. GIP had an augmenting effect on amylase and volume secretion from the pancreas, when pancreatic secretion was stimulated by 2.5 X 10(-6) M Ach, but not by 0.05 or 0.25 X 10(-6) M. Exogenous rat insulin could exert an effect similar to that of GIP, although a higher dose was required. Atropine inhibited the effect of Ach on exocrine and endocrine pancreatic secretion, but not the insulinotropic action of GIP. It is hypothesized that GIP could play a role in regulating exocrine pancreatic secretion by its insulinotropic action.

Acetylcholine↗
PubMed1986

Effect of calcitonin on the interdigestive motility and on gastric and pancreatic secretion in humans.

Calcitonin given in doses (0.2 and 1 MRC U/kg-1h-1) reproducing the levels observed in medullary carcinoma of the thyroid, induced the appearance of phase III type activity and reduced the duration of the IMC in the small intestine from 123 to 87 min with 0.2 MRC U kg-1h-1 and from 123 to 43 min with 1 MRC U kg-1h-1 but not in the stomach of young volunteers. This increase in phase III-like activity occurred despite a sharp reduction in motilin levels. Only the highest dose of calcitonin reduced significantly acid secretion (by more than 90%) while both doses reduced amylase secretion by respectively 65 and 71% when compared to the control levels. These changes in motility and secretion could partly explain the diarrhea observed in patients with the medullary carcinoma of the thyroid.

Adolescent↗
PubMed1986

Gastrointestinal toxicity. Role of prostaglandins and leukotrienes.

Gastrointestinal tissues have a high synthesising capacity for prostaglandins. As exogenous prostaglandins protect the gastrointestinal mucosa against potentially noxious agents, it has been suggested that the generation of prostaglandins plays a crucial role in the maintenance of mucosal integrity. Analgesic and anti-inflammatory drugs with a potent inhibitory action on gastrointestinal cyclo-oxygenase, such as indomethacin, induce gastric and intestinal ulcerations in experimental animals and frequently lead to gastrointestinal side effects in man. However, drugs that do not reduce gastrointestinal prostaglandin formation, such as paracetamol (acetaminophen), are devoid of gastrointestinal toxicity. Various factors, e.g. tissue-specific differences in the sensitivity of cyclo-oxygenase against inhibition and pharmacokinetic properties, modify the inhibitory activity of analgesic and anti-inflammatory drugs on gastrointestinal prostaglandin formation. As leukotriene C4 is a potent gastric vasoconstrictor, increased metabolism of arachidonic acid via the 5-lipoxygenase pathway in the presence of inhibition of cyclo-oxygenase could possibly contribute to drug-induced gastrointestinal damage.

Animals↗
PubMed1983

Glucose-dependent insulinotropic action of cholecystokinin octapeptide in the isolated perfused rat pancreas.

Whether cholecystokininoctapeptide (CCK-8) stimulates insulin secretion at submaximal or supramaximal levels for pancreatic exocrine secretion was investigated. CCK-8 was delivered to the isolated perfused rat pancreas by a linear gradient ranging from 0 to 1,100 or 0 to 220 pg/ml at two different glucose concentrations. At 2.8 mM glucose CCK-8 was not insulinotropic even at supramaximal stimulation for exocrine pancreatic secretion. At 15.8 mM glucose CCK-8 was insulinotropic starting already at concentrations which were submaximal for stimulation of exocrine pancreatic secretion. It was concluded that CCK-8 warrants consideration as a hormone involved in the enteroinsular axis.

Animals↗