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M Classen

Publications and source records attributed to M Classen.

At least 163 records · Page 9Linked to original sources
PubMed1991

GLP-1-(7-36) amide, -(1-37), and -(1-36) amide: potent cAMP-dependent stimuli of rat parietal cell function.

We investigated the effect of glucagon-like peptide 1 (GLP-1)-(7-36) amide and its molecular variants GLP-1-(1-37) and GLP-1-(1-36) amide on enzymatically dispersed enriched rat parietal cells using [14C]aminopyrine accumulation as a measure of H+ production. GLP-1-(7-36) amide was 100 times more potent than GLP-1-(1-37) and GLP-1-(1-36) amide in stimulating [14C]aminopyrine accumulation. At their maximally effective concentrations, GLP-1-(7-36) amide (10(-8) M), GLP-1-(1-37) (10(-6) M), and GLP-1-(1-36) amide (10(-6) M) reached 80-90% of the response to 10(-4) M histamine. However, the peptides were 100-10,000 times more potent than histamine, which induced maximal [14C]aminopyrine accumulation at 10(-4) M. Stimulation by GLP-1 was dependent on the presence of a phosphodiesterase inhibitor and was not altered by pertussis toxin. Ranitidine failed to affect the response to the GLP-1 variants. Stimulation of H+ production by GLP-1 was accompanied by an increase in the formation of adenosine 3',5'-cyclic monophosphate (cAMP) but not by changes in phosphoinositol breakdown. In stimulating [14C]aminopyrine accumulation, the GLP-1 variants acted additively to threshold but not to maximal concentrations of histamine, suggesting that histamine and GLP-1 activate the same cAMP pool. In contrast, in anesthetized rats GLP-1-(7-36) amide (10-500 ng.kg-1.h-1) had no effect on basal and pentagastrin-stimulated acid secretion in vivo. We conclude that GLP-1 exerts a direct stimulatory effect on rat parietal cells. This potent effect is mediated by cAMP and is independent of H2 receptors. In vivo direct stimulation by GLP-1 of the parietal cells might be counterbalanced by indirect inhibitory mechanisms that are excluded in the in vitro cell system.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Modulatory effect of insulin on rat small intestinal motility and peptide release in vitro.

Intact segments of rat ileum were stimulated in vitro by either electrical field stimulation (EFS) or cholinergic stimulation with carbachol, in the presence of absence of varying insulin concentrations (50, 100 and 200 microU/ml), and the contraction in the longitudinal axis was recorded. Insulin had no significant influence on the carbachol contractile dose-response curve nor did it affect the cholinergically mediated 'on-contraction' at onset of the electrical stimulus. The 'off-contraction' occurring at cessation of the electrical stimulus was partly mediated by a cholinergic and partly by a noncholinergic and nonadrenergic mechanism, and decreased over time with repeated stimulation. This decay with time was significantly attenuated by insulin. In the presence of insulin, release of bombesin-like immunoreactivity induced by carbachol or EFS significantly increased. On the other hand, the release of somatostatin-like immunoreactivity was suppressed by 50-70% in the presence of insulin. These results demonstrate that in vitro insulin can modify both the motility responses of isolated segments of rat ileum and the neuropeptide release from such segments.

Animals↗
PubMed1991

Substitution of factor XIII: a therapeutic approach to ulcerative colitis.

Three patients with ulcerative colitis in the active stage demonstrated reduced levels of F XIII activity and F XIII subunit A (61 and 80.3%, respectively). Because of the lack of clinical improvement during conservative therapy, the patients were treated additionally with F XIII concentrate (Fibrogammin HS, Behring, FRG) for 10 days. The substitution resulted in an increase in F XIII activity (144.3%) and F XIII subunit A (238%) as well as in a marked improvement in symptoms.

Adrenal Cortex Hormones↗
PubMed1991

Effect of motilin on gastric emptying in patients with diabetic gastroparesis.

OBJECTIVES: Because disturbances of gastric emptying are a serious complication in insulin-dependent diabetic subjects with regard to the maintenance of good metabolic control, we wanted to assess the effectiveness of motilin as a potential treatment for gastric emptying disturbances. RESEARCH DESIGN AND METHODS: The intestinal hormone motilin has been shown to accelerate gastric emptying in healthy subjects. Therefore, we examined the effect of intravenous motilin on gastric emptying of a 99mTc colloid-labeled semisolid test meal in 9 insulin-dependent diabetic patients with diabetic gastroparesis. All patients had a significantly delayed gastric emptying rate compared with a group of 11 healthy control subjects. RESULTS: During the infusion of motilin, gastric emptying was accelerated, and it was no longer significantly different from control values. CONCLUSIONS: These data demonstrate that motilin and related compounds such as erythromycin derivatives could be useful for the treatment of disturbed gastric emptying in diabetic subjects.

Adult↗
PubMed1991

Effect of CCK on food intake in man: physiological or pharmacological effect?

The present study was designed to determine in humans the dose of CCK which suppresses food intake. 18 male subjects received in randomized order either i.v. saline or Thr28 Nle31 CCK 25-33 (CCK-9) at 100 or 500 pmol/kgh, respectively. In addition, 7 subjects received CCK together with the opiate receptor antagonist naloxone to examine if activation of endogenous opioids might interfere with the potential satiating effect of CCK. Food intake during saline was 32 +/- 2 sandwiches (mean +/- SEM), during CCK-9 100 pmol/kgh 28 +/- 2 (n.s.) and only 12 +/- 3 during CCK-9 500 pmol/kgh (p less than 0.01). The respective water intake was 730 +/- 70 ml, 590 +/- 60 ml (n.s.) and 320 +/- 50 ml (p less than 0.01). Naloxone further reduced food and water intake during high but not low dose CCK or saline. During saline postprandial insulin levels rose by 49 +/- 6 microU/ml within 45 min which was attenuated during low dose (23 +/- 6 microU/ml; p less than 0.01) and high dose CCK-9 (1 +/- 1 microU/ml; p less than 0.001). Plasma glucagon did not change in control or CCK experiments. The postprandial rise of pancreatic polypeptide was attenuated during high dose CCK. Naloxone had no effect on the hormonal response except for a prolonged reduction of insulin and glucose levels following high dose CCK + naloxone. Plasma CCK levels rose by 5.4 pmol/l in controls but by 55 and 255 pmol/l during the low and high dose CCK infusion, respectively. These data demonstrate that suppression of food intake in man by i.v. CCK is a pharmacological rather than a physiological effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[Self-expanding and expandable bile duct prostheses].

The main problem of conventional endoscopic or percutaneous biliary drainage is the clogging of plastic endoprostheses. Therapeutic advances may be achieved by self-expanding or balloon-expandable braided or slit metal stents due to their large lumen and small surface area. Preliminary clinical studies show excellent early results but a divergent long-term clinical outcome depending on the selection of patients, the implantation technique or the type of the stent. If a long-distance overlap of biliary stenoses is achieved the metal stents may be superior to plastic prostheses due to a reduction of the risk of bile encrustation.

Bile Duct Neoplasms↗
PubMed1991

[Indications and value of endosonography of the upper gastrointestinal tract].

Endoscopic ultrasound (EUS) has been used in the diagnosis and staging of gastroenterologic tumors for about ten years. High accuracy rates of EUS in staging of esophageal, gastric and pancreatic carcinoma (T-stage: 80-95%, N-stage: 75-85%) have been reported. EUS is therefore a valuable diagnostic tool für assessment of prognosis as well as for planning of therapy of these tumors. Its value in benign gastroenterologic disease is unclear. EUS seems to be much less reliable in the differentiation between benign and malignant changes (e.g. esophageal stenoses, gastric ulcers, pancreatic mass lesions).

Bile Duct Neoplasms↗
PubMed1991

[Diabetes mellitus and arterial hypertension. In search of the connecting link].

Late diabetic effects are the sequelae of for a long time super elevated blood sugar levels. The diabetic nephropathy is the cause of the secondary arterial hypertension. The investigation seeks for the connections between the diabetes mellitus and the essential, that is primary hypertension. The two diseases frequently appear and clearly increase in the second half of life. Moreover, they are above average frequently associated with each other. Among brothers and sisters of diabetic hypertensives in comparison to normal cohorts clearly increased high blood pressure prevalences were found. The insulin resistance which could be proved in a great number of hypertensive and which has been known since more than two decades might be the connecting link between hypertension and diabetes mellitus. Like the obesity the essential hypertension can be associated with all degrees of an insulin hyposensitiveness. The sodium-retaining effect of the insulin might explain the increased sodium content of the body in hypertensives. The differential diagnostics of the essential hypertension should therefore seek for conditions of an insulin resistance. The type II diabetic lacks a release of bradykinin during muscle work. Thus the glucose uptake into the cell is unfavourable influenced and demands an increased insulin excretion. This genetically (?) fixed defect is found also in essential hypertensives. It could be the connecting link between the two diseases. ACE-inhibitors have via a kininase II inhibition an effect also on the bradykinin decomposition and can favourable influence the glucose uptake into the muscle. An improved insulin effect among the ACE-inhibitors was described. Therefore, they should be preferred in the treatment of hypertensive diabetics.

Diabetes Mellitus, Type 2↗
PubMed1991

Effect of intraduodenal or intragastric nutrient infusion on food intake in man.

In man, only little is known about the site of origin of satiety signals within the gastrointestinal tract. Therefore, it was the aim of this study to examine the role of the stomach and the small intestine as a source of satiety signals. 8 overnight fasted healthy volunteers received intraduodenal (100 or 200 ml/h) or intragastric (100 ml/h) infusions of a mixed liquid diet (Biosorb) or iso-osmolar saline, respectively. 20 minutes after start of the infusion, standardized mini-sandwiches and water were presented and food intake was recorded for the ensuing 90 minutes. During both rates of intraduodenal nutrient infusion, cumulative food intake was identical to that during saline infusion. However, during intragastric nutrient infusion, cumulative food intake was significantly reduced compared to saline infusion (30 +/- 1 vs. 36 +/- 2 sandwiches; p less than 0.05). These data indicate that food consumption in man is reduced, if initiation of eating is preceded by nutrient administration into the stomach, but not into the duodenum. This effect does not appear to be mediated by gastrin, since plasma gastrin levels were not different during gastric and duodenal nutrient administration. In conclusion, the results of this study suggest that the generation of satiety signals in man is dependent on the presence of food in the stomach. Food only in the duodenum has no effect, although synergistic gastric and intestinal mechanisms can as yet not be excluded.

Adult↗
PubMed1991

Phenotypic and functional characterization of human TCR gamma delta+ intestinal intraepithelial lymphocytes.

Intestinal intraepithelial lymphocytes (IEL) appear to represent a peculiar set of immune cells compartmentalized at the interface between the organism and the external environment. In previous studies we observed that within human IEL TCR-tau/delta T cells represent a major fraction that predominantly express the CD8 molecule and preferentially uses the V-delta-1 gene segment. Thus these data suggested a preferential accumulation/homing of CD8+ V-delta-1+ IEL within the human intestinal epithelium. However, to date the functional role of these cells with regard to immune regulation at this most critical immunological site is poorly understood. In this study, the cytotoxic potential and proliferative capacity of human IEL in response to mitogenic stimuli has been characterized with respect to IEL T cell receptor type and TCR-tau/delta variable gene segment usage as determined by flowmetry. The frequency of TCR-1+ IEL expressing both CD56 and CD16 which are considered to be NK-cell markers was found to be much higher (38.9 +/- 12.4%) than within intestinal lamina propria lymphocytes (LPL) (9.1 +/- 4.8%) or peripheral blood lymphocytes (PBL) (6.4 +/- 3.3%). In contrast, the fractions of CD16-CD56+ cells within IEL, LPL and PBL were comparable. Surprisingly, IEL mediated NK-cell activity (K562 lysis) was virtually absent whereas within PBL it was within the normal range. Furthermore, in cytotoxicity assays employing 51Cr-labeled OKT3 hybridoma cells and P815 cells as targets, the cytotoxic potential of IEL was much lower than that of PBL.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Interaction of trimebutine and Jo-1196 (fedotozine) with opioid receptors in the canine ileum.

Receptor binding of the opioid receptor antagonist, [3H]diprenorphine, which has a similar affinity to the various opioid receptor subtypes, was characterized in subcellular fractions derived from either longitudinal or circular smooth muscle of the canine small intestine with their plexuses (myenteric plexus and deep muscular plexus, respectively) attached. The distribution of opioid binding activity showed a good correlation in the different fractions with the binding of the neuronal marker [3H]saxitoxin but no correlation to the smooth muscle plasma membrane marker 5'-nucleotidase. The saturation data (Kd = 0.12 +/- 0.04 nM and maximum binding = 400 +/- 20 fmol/mg) and the data from kinetic experiments (Kd = 0.08 nmol) in the myenteric plexus were in good agreement with results obtained previously from the circular muscle/deep muscular plexus preparation. Competition experiments using selective drugs for mu [morphiceptin-analog (N-MePhe3-D-Pro4)-morphiceptin] ), delta (D-Pen2,5-enkephalin) and kappa (dynorphin 1-13, U50488-H) ligands showed the existence of all three receptor subtypes. The existence of kappa receptors was confirmed in saturation experiments using [3H] ethylketocycloazocine as labeled ligand. Two putative opioid agonists, with effects on gastrointestinal motility, trimebutine and JO-1196 (fedotozin), were also examined. Trimebutine (Ki = 0.18 microM), Des-Met-trimebutine (Ki = 0.72 microM) and Jo-1196 (Ki = 0.19 microM) displaced specific opiate binding. The relative affinity for the opioid receptor subtypes was mu = 0.44, delta = 0.30 and kappa = 0.26 for trimebutine and mu = 0.25, delta = 0.22 and kappa = 0.52 for Jo-1196. Thus, Jo-1196 had some selectivity for kappa receptors compared to trimebutine. We conclude that there are similar types of opioid receptors in the myenteric plexus and the deep muscular plexus and that specificity of function of opioid nerves must depend on differential location of receptor types on particular neurons. The action of trimebutine and related drugs could vary depending upon their interactions with various gut opioid receptors having different physiological roles.

5'-Nucleotidase↗
PubMed1991

[Endoscopic ultrasound in small pancreatic tumors].

32 of 89 pancreatic tumors examined by endoscopic ultrasonography (EUS) from January 1986 to February 1990 had a diameter of 3 cm or less. The final diagnosis of a malignant (n = 28) or benign (n = 4) pancreatic neoplasma was achieved by operation, puncture or autopsy. The accuracy of EUS (100%) was higher than for ultrasound (61%), computed tomography (64%) or endoscopic-retrograde cholangiopancreatography (84%). The echopattern of the small pancreatic carcinomas showed, compared to larger neoplasms, less often regressive changes (21 vs. 77%) and a well demarcated or smooth tumor margin (25 vs. 2%). However, it is not possible to differentiate reliably a small malignant from a benign pancreatic tumor by the echofeatures alone. Since most pancreatic tumors are large at the time of clinical presentation, they can be visualized by conventional imaging methods in most cases. EUS adds clinically important information to the diagnosis of pancreatic carcinoma especially in small tumors.

Cholangiopancreatography, Endoscopic Retrograde↗
PubMed1990

[Sonographic percutaneous drainage of liver abscesses].

13 patients with pyogenic liver abscess and five patients with amoebic abscess underwent percutaneous drainage of the abscesses using the Seldinger (n = 8) or trocar technique (n = 11). The results showed that the trocar method was easier and faster to perform and well tolerated by the patients. No complications were observed despite of one case of transient peritonitis caused by a dislocated catheter. One patient with pyogenic liver abscess died of septic shock. All other patients were successfully treated, using local drainage and systemic antibiotic therapy.

Aged↗
PubMed1990

Vagally induced release of gastrin, somatostatin and bombesin-like immunoreactivity from perfused rat stomach. Effect of stimulation frequency and cholinergic mechanisms.

The isolated stomach of rats was vascularly perfused to measure the secretion of gastrin, somatostatin (SLI) and bombesin-like immunoreactivity (BLI). The gastric lumen was perfused with saline pH 7 or pH 2, and electrical vagal stimulation was performed with 1 ms, 10 V and 2, 5 or 10 Hz, respectively. Atropine was added in concentrations of 10(-9) or 10(-7) M to evaluate the role of cholinergic mechanisms. In control experiments, vagal stimulation during luminal pH 2 elicited a significant increase of BLI secretion only at 10 Hz but not at 2 and 5 Hz. Somatostatin release was inhibited independent of the stimulation frequency employed. Gastrin secretion at 2 Hz was twice the secretion rates observed at 5 and 10 Hz, respectively. At luminal pH 7 BLI rose significantly at 5 and 10 Hz. SLI secretion was decreased by all frequencies. Gastrin secretion at 2 and 5 Hz was twice as high as during stimulation with 10 Hz. Atropine at doses of 10(-9), 10(-8), 10(-7) and 10(-6) M had no effect on basal secretion of BLI, SLI and gastrin. At luminal pH 2, atropine increased dose-dependently the BLI response at 2 and 5 but not at 10 Hz. The decrease of SLI during 2 and 5 Hz but not 10 Hz was abolished by atropine 10(-9) M. SLI was reversed to stimulation during atropine 10(-7) M at all frequencies. The rise of gastrin at 2 Hz was reduced by 50%. At luminal pH 7, atropine had comparable effects with a few differences: the BLI response at 10 Hz was augmented and the gastrin response to 2 and 5 Hz was reduced. In conclusion the present data demonstrate a frequency and pH-dependent stimulation of BLI and gastrin release. The stimulation of BLI is predominantly due to atropine-insensitive mechanisms while muscarinic cholinergic mechanisms exert an inhibitory effect on BLI release during lower stimulation frequencies (2 and 5 Hz) independent of the intragastric pH and also during higher frequencies at neutral pH. Both, atropine sensitive and insensitive mechanisms are activated frequency dependent. The atropine-sensitive cholinergic mechanisms but not the noncholinergic mechanisms involved in regulation of G-cell function are pH and frequency dependent. Somatostatin is regulated largely independent of stimulation frequency and pH by at least two pathways involving cholinergic mechanisms of different sensitivity to atropine. These data suggest a highly differentiated regulation of BLI, gastrin and SLI secretion and the interaction between these systems awaits further elucidation.

Animals↗