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Biomedical subjects

S Raptis

Publications and source records attributed to S Raptis.

At least 163 records · Page 9Linked to original sources
PubMed1977

Inhibition of cholecystokinin-pancreozymin release by somatostatin.

To determine the effect of somatostatin on cholecystokinin-pancreozymin (C.C.K.) release, serum-C.C.K. concentrations were measured in normal volunteers after intraduodenal olive oil, with and without a simultaneous intravenous infusion of somatostatin. After instillation of the olive oil there was a rapid rise in serum-C.C.K. (integrated response 19 682+/-5632 pg min ml-1). This rise was completely abolished by somatostatin (integrated response -373+/-330 pg min ml-1, P less than 0-005) and rebound hyper-secretion was seen after the infusion had been stopped. These findings indicate that somatostatin may be involved in regulating C.C.K. release after meals, and suggest a possible explanation for the profound steatorrhoea seen in a patient with a somatostatin-producing tumour.

Adult↗
PubMed1977

Concentrations of prostaglandin A-, E- and F-like substances in gastric mucosa of normal subjects and of patients with various gastric diseases.

1. Prostaglandin A-, prostaglandin E- and prostaglandin F-like substances were determined radioimmunologically in antral biopsy material obtained by endoscopy. 2. In patients with gastritis, the concentrations of prostaglandin (E+A)-like substances were six times as high and of prostaglandin F-like substances twice as high as in normal subjects. In chronic atrophic gastritis, the concentrations of prostaglandin (E+A)-like material was four times as high as in normal subjects whereas prostaglandin-F like material remained unchanged. In acute gastric ulcer, prostaglandin (E+A)-like material reached concentrations four times times higher than in normal subjects, accompanied by a fivefold increase of prostglandin F-like substances. After healing of the gastric ulcer, prostaglandins returned to normal values. 3. There was no correlation between gastrin and prostaglandins in all biopsy specimens.

Adult↗
PubMed1977

Prevention by somatostatin of rise in blood pressure and plasma renin mediated by beta-receptor stimulation.

The interrelationships of increased plasma renin and elevated blood pressure following acute beta-stimulation by orcipernaline and its prevention by somatostatin was studied in normal man. During somatostatin infusion basal values of renin and blood pressure were unchanged. Following orciprenaline both variables increased significantly. Combination of somatostatin and orciprenaline reduced the rise in plasma renin activity by 49%, mean arterial blood pressure by 21% and heart rate by 19%, compared with beta-stimulation alone. The results indicate that the inhibitory action of somatostatin on plasma renin activity may be mediated via beta-receptors. The lesser increase of blood pressure under somatostatin plus orciprenaline also indicates a possible inhibitory effect of somatostatin on beta-adrenergic receptors.

Adult↗
PubMed1977

Effects of somatostatin and human gastrin I on the lower esophageal sphincter in man.

The influence of gastrin and somatostatin on the lower esophageal sphincter was investigated in a total of ten metabolically healthy volunteers and one patient with Zollinger-Ellison syndrome. It could be shown that only unphysiologically high concentrations of gastrin produce a rise in pressure in the lower esophageal sphincter, while somatostatin has neither an effect on the lower esophageal sphincter pressure, nor is it able to inhibit the pharmacological effect of exogenic gastrin administration. The results of this study demonstrate that normal levels of serum gastrin do not seem to have much effect of resting LES pressure, nor does somatostatin. (Gastrin, in fact, in pharmacologic dosage does have an effecton the tonicity of the lower esophageal sphincter.)

Adult↗
PubMed1977

Somatostatin modulation of pancreatic glucagon, insulin, glucose and free fatty acids following beta-adrenergic stimulation.

This study was undertaken to determine the effect of somatostatin on acute, orciprenaline mediated, beta-adrenergic stimulation of free fatty acids, blood glucose, insulin, and glucagon in healthy subjects. After orciprenaline and somatostatin insulin and glucagon decreased, whereas blood glucose and free fatty acids increased, probably in part as a result of the lesser inhibition of glucagon (50%) than of insulin (83%). From these observations it is tentatively concluded that the inhibitory effects of somatostatin on insulin and glucagon release in man are a consequence of beta-adrenergic receptor involvement. These effects are possibly mediated through increased destruction of cAMP, blocking of camp dependent secretion or impairment of calcium uptake.

Adult↗
PubMed1977

The effect of somatostatin on platelets: in vivo and in vitro studies.

The influence of somatostatin on platelets was studied in healthy volunteers. After a bolus injection of 250 microgram somatostatin followed by a three hour infusion at a rate of 250 microgram somatostatin/hr a statistically significant fall of platelet count and impairment of platelet aggregation was observed. The aggregation inhibiting effect of somatostatin at the end of the three hour infusion is clinically unimportant as compared to the effect of aspirin. In vitro concentrations up to 10.0 microgram somatostatin per ml do not show any effect on platelet aggregation and platelet stickiness. Endocrinologically active doses of somatostatin in short term infusions are very unlikely to cause bleeding disorders.

Adolescent↗
PubMed1976

Prevention of stress ulcer by somatostatin in rats.

In animal experiments it was examined, to what extent prophylactic application of Somatostatin is able to prevent the stress-induced ulcer of the rat. 32 male Wistar rats were exposed to a combined immobilisation-hypoxia-stress. Somatostatin was given intraperitoneally as bolus and intravenously as a continuous infusion. The results indicated that Somatostatin lowers significantly the incidence rate of stress-induced gastric ulcers in the rat.

Animals↗
PubMed1976

Coagulation studies and platelet function after somatostatin infusion.

The effect of short- and long-term somatostatin (GIF) administration on haemostatic function in man was investigated. The dosage programme applied in this study was 250 mug GIF as a bolus injection and 250 mug GIF/h by way of infusion. In five healthy volunteers a short-term (3h) treatment resulted in a statistically significant drop of platelet count and impairment of platelet aggregation at the end of infusion. However, these changes were within the physiologically normal range and disappeared after two hours on all subjects. Other parameters such as bleeding time, thromboplastin and partial thromboplastin time, fibrinogen, fibrin/fibrinogen split products, plasma factor XIII, ethanol gelation test were not affected. In two patients with gastric haemorrhage and persistent amylasaemia a 67 or 120-h treatment induced no remarkable haemostatic defect. By contrast, peptic ulcer bleeding in one patient stopped 60 min after starting the GIF infusion. These studies indicated that somatostatin administration in man at the dosage programme used neither results in clinical evidence indicating bleeding tendency nor does it influence laboratory parameters in an apparent way.

Adult↗
PubMed1976

Human C-peptide. Part II: Clinical studies.

Human C-peptide is determined by radioimmunoassay. On gel filtration of serum from a healthy subject and from a patient with islet cell carcinoma, C-peptide (MW 3025) appears ahead of insulin (MW 5808) and shows much higher molar concentrations than the hormone. Human proinsulin cross-reacts with our antiserum to synthetic human C-peptide. On direct determination of immunomeasurable C-peptide (IMCP) in fasting serum of 25 healthy subjects we find an average of 1.8 (+/- 0.4) ng/ml, corresponding to 60.4 X 10(-11) Mol/l. The molar concentration is about five-fold as compared to IMI (immuno-measurable insulin). IMCP and IMI patterns are not identical on stimulation of beta-cell secretion in healthy subjects by i.v. glucose or glucose-glibenclamide. This is probably due to differences in peripheral metabolism of both compounds. We conclude from our results that C-peptide determined in peripheral venous serum is a better indicator of beta-cell secretion than is insulin. Among 26 insulin-treated juvenile diabetics 15 show not measurable and 11 subnormal IMCP levels in fasting serum. No rise in IMCP is found 1-2 h following breakfast. Four juvenile patients receiving no insulin in a phase of total diabetes remission have normal or raised fasting IMCP concentrations. Only 2 out of 24 adult diabetics (16 treated with insulin and 8 with tablets) show non-measurable fasting IMCP concentrations, in another 4 patients values are below and in the remaining 18 cases above 1 ng/ml serum. Stimulation of beta-cell secretion through glucose-glibenclamide is more or less impaired in all adult diabetics compared to the healthy subjects.

C-Peptide↗
PubMed1976

Inhibition of frusemide-induced hyperreninaemia by growth-hormone release-inhibiting hormone in man.

In a study of the effect of somatostatin (growth-hormone release-inhibiting hormone) on plasma-renin in healthy volunteers, plasma-renin activity was measured by radioimmunoassay after the intravenous administration of somatostatin and also during frusemide-induced hyperreninaemia. While somatostatin was being given, basal values of renin were unchanged. Injection of frusemide alone produced hyperreninaemia; but, under somatostatin, renin release was inhibited by 45%. The results indicate that somatostatin is a potent inhibitor of renin and exerts its effect independent of sodium excretion, which was unchanged under somatostatin. Conceivably, somatostatin plays an important role in the regulation of endogenous renin release.

Adult↗
PubMed1976

Somatostatin: a potent inhibitor of ACTH-hypersecretion in adrenal insufficiency.

Somatostatin (250 mug as a bolus i.v. and 250 mug as a 1-hr infusion) was administered to 5 patients with adrenal insufficiency of different origin. In each patient a sustained, progressive fall in plasma ACTH was observed during the infusion period. The mean maximal reduction in plasma ACTH was 43.8 +/- 5.9%. After cessation of the somatostatin infusion there was a rise of plasma ACTH to starting levels within 1/2 hour. These findings suggest that somatostatin is a potent inhibitor of ACTH secretion, however, only in a condition in which glucocorticoids are lacking.

Addison Disease↗
PubMed1976

Hypergastrinemia induced by glucocorticoid and corticotropin treatment in man.

To elucidate further the pathogenesis of steroid-induced ulceration, plasma gastrin levels, both basal and after a test meal, were studied in normal volunteers and patients treated with glucocorticoids or corticotropin. In normal subjects the acute intravenous administration of 100 mg prednisolone had no effect on plasma gastrin levels. After oral administration of prednisolone (40 mg daily, for four days) a significant increase of the basal, the reactive, and the over 90-min integrated gastrin release was observed. In this group, the glucocorticoid treatment had a slight, but significant influence on gastric acid and pepsin secretion, while acidity and pepsin output stimulated by pentagastrin was not affected. In patients treated with prednisolone for more than 24 weeks, the oral administration of this hormone failed to alter basal gastrin values but affected significantly secretion after the test meal. In patients with multiple sclerosis, after intramuscular administration of corticotropin (60 IU daily, for 12 days), an increase of the basal, the reactive, and the integrated gastrin release also was found. Glucocorticoid-induced hypergastrinemia provides information on the pathogenesis of steroid-induced ulceration.

Adolescent↗