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Biomedical subjects

F Stöckmann

Publications and source records attributed to F Stöckmann.

At least 55 records · Page 3Linked to original sources
PubMed1987

Xenopsin- and neurotensin-like peptides in gastric juice from patients with duodenal ulcers.

Using an anti-serum directed against the COOH-terminal region of neurotensin and an anti-serum raised xenopsin in radioimmunoassays, the presence of neurotensin- and xenopsin-like immunoreactivity in Sep-pak extracts of human gastric juice was demonstrated. An anti-serum directed against the NH2-terminal to central residues of neurotensin and an anti-serum directed against a conformation, present only in the intact peptide, did not detect immunoreactivity in the juice. Infusions of pentagastrin at doses of 0.75 micrograms kg-1 h-1 and 1.5 micrograms kg-1 h-1 resulted in significant (P less than 0.05) increases in the total amount of xenopsin-like, but not neurotensin-like, immunoreactivity released in the juice compared with basal release. No significant differences in the release of xenopsin- or neurotensin-like immunoreactive were observed between patients with selective proximal vagotomy and patients without operation. Analysis by gel permeation chromatography and high performance liquid chromatography demonstrated that both the neurotensin- and xenopsin-like immunoreactivity was heterogeneous and an increase in molecular complexity on pentagastrin-stimulation was observed. As both neurotensin and xenopsin inhibit gastric exocrine activity, the presence of immunochemically related substances in gastric juice may have physiological relevance.

Chromatography, Gel↗
PubMed1987

Circulating tachykinins (substance P, neurokinin A, neuropeptide K) and the carcinoid flush.

Antisera of defined regional specificity have been used to measure the concentration of substance P-like immunoreactivity (SP-LI) and neurokinin A-like immunoreactivity (NKA-LI) during a meal-induced flush in 10 patients with metastatic carcinoid tumours. Although all patients flushed, NKA-LI levels in five patients and SP-LI in six patients were not elevated relative to healthy subjects (NKA-LI, less than 3 pg/ml; SP-LI, less than 10 pg/ml) both in the fasted state and after food. In the patients with elevated basal plasma tachykinin levels, increases in NKA-LI and SP-LI after food were erratic and did not correspond to a defined digestive phase or the occurrence of the flush. Chromatographic analysis of plasma demonstrated the presence of neuropeptide K and neurokinin A, and the detection of COOH-terminal fragments of substance P is consistent with the higher levels of circulating SP-LI measured with a COOH-terminally directed antiserum compared with an NH2-terminally directed antiserum. Subcutaneous injection of the somatostatin analogue SMS 201-995 (50 micrograms) alleviated symptoms of flush in two of three patients but only partially suppressed NKA-LI and SP-LI concentrations. It is concluded that circulating tachykinins cannot be solely responsible for the meal-induced carcinoid flush.

Adult↗
PubMed1986

Reduced incretin effect in type 2 (non-insulin-dependent) diabetes.

Integrated incremental immunoreactive insulin and connecting peptide responses to an oral glucose load of 50 g and an "isoglycaemic" intravenous glucose infusion, respectively, were measured in 14 Type 2 (non-insulin-dependent) diabetic patients and 8 age- and weight-matched metabolically healthy control subjects. Differences between responses to oral and intravenous glucose administration are attributed to factors other than glucose itself (incretin effect). Despite higher glucose increases, immunoreactive insulin and connecting peptide responses after oral glucose were delayed in diabetic patients. Integrated responses were not significantly different between both groups. However, during "isoglycaemic" intravenous infusion, insulin and connecting peptide responses were greater in diabetic patients than in control subjects as a consequence of the higher glycaemic stimulus. The contribution of incretin factors to total insulin responses was 72.8 +/- 6.9% (100% = response to oral load) in control subjects and 36.0 +/- 8.8% in diabetic patients (p less than or equal to 0.05). The contribution to connecting peptide responses was 58.4 +/- 7.6% in control subjects and 7.6 +/- 14.5% (p less than or equal to 0.05) in diabetic patients. Ratios of integrated insulin to connecting peptide responses suggest a reduced (hepatic) insulin extraction in control subjects after oral as compared to intravenous glucose. This was not the case in diabetic patients. Immunoreactive gastric inhibitory polypeptide responses were not different between control subjects and diabetic patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Serotonin release into blood after food and pentagastrin. Studies in healthy subjects and in patients with metastatic carcinoid tumors.

The effect of a 550-kcal mixed meal and of an intravenous injection of pentagastrin (0.06 microgram/kg body wt) upon peripheral blood serotonin concentrations has been compared in 10 carcinoid patients with hepatic metastases and healthy subjects. The fasting concentrations of blood serotonin in the patients (range 790-4500 ng/ml) were elevated compared with healthy subjects (range 71-310 ng/ml; n = 15). Urinary output of 5-hydroxyindole acetic acid was elevated in 8 patients but was in the healthy range for 2 patients. The healthy subjects (n = 9) responded to food with an increase in blood serotonin (maximum rise over mean basal of 32% +/- 4%) that was significant at 60, 75, 90, and 105 min postcibal. All carcinoid patients responded to food with a comparable (25% +/- 11% over basal) rise in serotonin but the pattern of release was erratic. All patients with tumor metastases exhibited symptoms of the carcinoid flush after eating, but there was no correlation between occurrence and severity of the flush and occurrence and magnitude of the rise in serotonin. Intravenous pentagastrin evoked a flush in all carcinoid patients, but there was no significant increase in peripheral blood serotonin either in the patients or in healthy subjects.

Adult↗
PubMed1986

Measurement and partial characterization of the multiple forms of neurokinin A-like immunoreactivity in carcinoid tumours.

An antiserum raised against neurokinin A has been used to demonstrate storage and release of neurokinin A-like immunoreactivity by carcinoid tumours. The antiserum showed reactivity towards members of the tachykinin family of polypeptides in the order: neurokinin A greater than eledoisin greater than neurokinin B greater than kassinin greater than substance P greater than physalaemin but the magnitude of the cross-reactivity with substance P and physalaemin was less than 1% of that of neurokinin A. A sensitive (IC50 238 fmol/ml; minimum detectable concentration, 9 fmol/ml) radioimmunoassay was set up using this antiserum. Extracts of metastatic tumour tissue from four patients with a primary carcinoid tumour in the midgut contained both neurokinin A-like immunoreactivity (NKA-LI) and substance P-like immunoreactivity (SP-LI). The concentrations (pmol/g wet weight) of NKA-LI and SP-LI in the tumours were: patient A 210, 201; patient B 2276, 6849; patient C 1198, 834 and patient D 424, 379. Analysis of the tumour extracts by reverse phase HPLC indicated that the NKA-LI was heterogeneous. Under two different conditions of chromatography, one component was eluted with the same retention time as neurokinin A. Two further components were more hydrophobic than neurokinin A but were not eluted with the retention time of neurokinin B. Analysis of these components by gel filtration indicated a molecular weight in the 3000-4000 range suggesting that they may be related to neuropeptide K, an N-terminally extended form of neurokinin A. NKA-LI and SP-LI were undetectable in the plasma of patients A and D but were elevated in patient B (NKA-LI 1005 +/- 114; SP-LI 345 +/- 85 fmol/ml) and patient C (NKA-LI 80 +/- 31; SP-LI 21 +/- 13 fmol/ml).

Carcinoid Tumor↗
PubMed1986

Effect of short- and long-term feeding of omeprazole on rat gastric endocrine cells.

Rats were tube-fed with omeprazole (40 mumol/kg body weight twice daily) for 30 and 60 days. As a result, fasting plasma gastrin levels were significantly elevated, while plasma somatostatin levels remained normal. Gastrin concentrations in the antral mucosa were unchanged after 30 days, but significantly elevated after 60 days. The relative stomach weight and the area of the antral and oxyntic mucosa increased significantly; however, the oxyntic mucosa thickness and the volume density of the parietal cells did not increase. Highly significant changes occurred in the endocrine cells of the antrum and corpus. The volume density of the argyrophilic (Grimelius technique) cells of the oxyntic mucosa increased time-dependently, and so did the volume density of the antral G cells, while the volume density of the antral D cells decreased. This resulted in a remarkable increase in the G/D cell ratio. All functional and morphological changes are reversed 42 days after omeprazole feeding for 60 days. The findings in the endocrine cells of the antral mucosa are explained by the omeprazole-induced permanent elevation of the intragastric pH and in the endocrine cells of the oxyntic mucosa by the following hypergastrinaemia.

Administration, Oral↗
PubMed1985

[Effect of a specific serine protease inhibitor on the rat pancreas. II. Influence of camostate on the endocrine pancreas].

Chronic oral administration of camostate, a specific serine protease inhibitor, is known to induce pancreas hypertrophy in rats. A possible influence of the protease inhibitor on the endocrine rat pancreas was studied using isolated perfused pancreas and islet incubations. The presence of camostate had no direct effect on the glucose-induced insulin release in vitro in concentrations from 1 microM to 1 mM, but enhanced the basal insulin release from islets cultured over 24 h in media containing the protease inhibitor (100 microM). Administration of camostate over 14 days to rats induced a remarkable hypertrophy of the pancreas without influencing plasma insulin or gastric inhibitory polypeptide levels and insulin concentration of the pancreas. Glucose-stimulated insulin release from the perfused pancreas was not increased despite significantly higher total insulin content. It is concluded that camostate exerts no direct effect on the glucose-stimulated insulin release and that chronic administration of the compound induces pancreas hypertrophy in vivo without influencing insulin release.

Administration, Oral↗
PubMed1984

Effect of a specific serine protease inhibitor on the rat pancreas: systemic administration of camostate and exocrine pancreatic secretion.

Camostate, a synthetic serine protease inhibitor, specifically inhibits the trypsin activity in vitro. Immediately after intravenous administration of camostate (5, 2.5, 0.5, and 0.1 mg/kg body weight/h) the trypsin activity in the biliary-pancreatic juice was diminished dose-dependently in anaesthetized rats. The amylase release was not influenced. Camostate and its metabolites were detected by high-pressure liquid chromatography in the pancreatic juice and tissue; in plasma, only the metabolites were found. Therefore, the inhibitory action of camostate on the trypsin activity in the biliary-pancreatic juice may be due to penetration of camostate into the juice.

Amylases↗
PubMed1984

Preceding hyperinsulinemia prevents demonstration of insulin effect on fat-induced gastric inhibitory polypeptide (GIP).

The effect of insulin on fat-induced gastric inhibitory polypeptide (GIP) release has been studied in seven healthy volunteers during euglycemic blood glucose clamping. In the first protocol, insulin (0.1 U/kg/h) was infused 2 h before ingestion of 100 g fat and continued for 2 h thereafter. In protocol II, saline was infused 2 h before the fat load and the insulin infusion started at the time of fat ingestion. During both insulin infusion studies, glucose levels were clamped at the fasting level by means of the Biostator and plasma levels of insulin, C-peptide, and GIP were estimated by radioimmunoassay. The response of GIP to oral fat was inhibited by 63% if insulin infusion was started at the time of fat ingestion, whereas no inhibition was seen if a 2-h hyperinsulinemic period preceded the fat load. The plasma insulin levels were comparable at the end of each experiment, ranging from 110 to 130 microU/ml. Plasma C-peptide levels decreased during the insulin infusion and increased after fat ingestion. These findings were not the result of inhibition of gastric emptying by insulin because they could be confirmed in four volunteers with intraduodenal infusion of fat. The present data show that insulin does inhibit fat-induced GIP secretion in normal man, but preceding hyperinsulinemic glucose clamping masks this insulin effect, probably by decreasing the sensitivity of the GIP cells to insulin.

Adult↗
PubMed1984

Hepatic artery embolization for treatment of endocrine gastrointestinal tumors with liver metastases.

We report about six patients with endocrine gastrointestinal tumors and liver metastases (four insulinomas, one carcinoidtumor, one paraganglioma), who were treated with a transluminal embolization of the hepatic artery when cytostatic therapy was ineffective. In two patients a second embolization was necessary after recurrence of clinical symptoms. All patients tolerated the procedure without severe side-effects and improved clinically. Serum insulin levels and HIAA-secretion rapidly decreased. Survival lasted from 3 to 32 months (median 15 months). Five additional patients with metastatic endocrine gastrointestinal tumors, observed during the same time period, were regarded as not suitable for hepatic artery embolization. In selected patients, hepatic artery embolization may become an effective therapy for treatment of metastasing endocrine gastrointestinal tumors when conventional medication with cytostatic drugs has become ineffective.

Adenoma, Islet Cell↗
PubMed1984

[Effect of FOY-305 on the activity and secretion of pancreatic enzymes in vitro].

FOY-305, a synthetic inhibitor of serin-proteases, shows a highly specific inhibition of the activity of purified trypsin and tryptic activity from duodenal juice in a range of 1 to 10 microM. Phospholipase A2 is only partly inhibited (40%) by much higher concentrations of FOY-305 (100 microM to 1 mM), amylase activity is not affected by either concentrations. FOY-305 did not influence CCK-stimulated amylase- and trypsin-secretion from isolated pancreatic lobules in concentrations which inhibited completely tryptic activity.

Amylases↗
PubMed1983

Disturbances of the entero-insular axis.

The entero-insular axis comprises direct substrate stimulation of the islet cells by the absorbed nutrients and signal transmission by endocrine factors and nerves. The extent of neural influences has not yet been evaluated. GIP is the main incretin candidate. GIP release is dependent on nutrient absorption. Therefore, GIP abnormalities occur in a large number of gastrointestinal and metabolic diseases. These secondary changes are rarely of clinical significance. GIP hypersecretion may, however, contribute to the increased lipogenesis in obesity and the hypoglycemia in the late dumping syndrome. In type II diabetes hyper- and hyposecretion of GIP has been found but no correlation between GIP and insulin response. GIP abnormalities are not identical with disturbances of the entero-insular axis. These can only be evaluated by estimating the incretin effect (comparing the insulin response to oral glucose with the insulin response to an isoglycaemic iv glucose infusion). A decreased incretin effect has been observed in patients with jejuno-ileal bypass and in type II diabetes. In neither condition was a correlation found between incretin effect and GIP response. It is concluded that disturbances of the entero-insular axis are rarely explained by GIP abnormalities. Therefore, other humoral gut factors must exist. Also the neural part of the entero-insular axis requires exploration in health and disease.

Animals↗
PubMed1982

[Criteria for diagnostic and therapeutic methods of vascular embolization (kidneys, spleen, liver) (author's transl)].

Basing on the findings in patients with extensive carcinomas of the kidneys, the article reports on the various possibilities of application of occlusion spirals (Gianturco's method), of injectable occlusion materials and a combinations of both methods. In the authors' own experience, the spiral technique has mostly proved successful in achieving embolization of the arteries of the kidney 24 hours before surgery. Both the spiral technique as well as the use of injectable emblizates and a combination of both are used in the treatment of macrohaematurias in non-operable kidney tumours. The article reports on the technical conditions, indication and methodical limitations of embolization of the splenic artery, basing on three actual cases. The conditions and technique of embolization of branches of the hepatic artery are discussed by means of the findings obtained in two patients with liver metastases of an insulinoma.

Adult↗