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Biomedical subjects

M Classen

Publications and source records attributed to M Classen.

At least 109 records · Page 6Linked to original sources
PubMed1995

Effect of human gastrin-17 with and without acid suppression on human esophageal motility.

The putative role of gastrin for the regulation of esophageal motility is a matter of debate. Accordingly it was the aim of this study a) to examine if physiological postprandial plasma levels of human gastrin-17 (hG-17) can affect esophageal motility, especially the pressure of the lower esophageal sphincter (LESP), and b) to assess the contribution of augmented acid secretion during gastrin infusion. In a first series of experiments postprandial plasma gastrin levels were determined in 8 healthy volunteers following the ingestion of a mixed meal. Gastrin rose from a baseline of 21 +/- 2 pg/ml to 67 +/- 8 pg/ml and returned almost to basal levels within 120 minutes. In a second experimental series the effect of i.v. synthetic human gastrin-17 (hG-17) was studied in 17 volunteers. At a lower dose of 0.75 ng/kg/min hG-17 increased plasma gastrin to 62 +/- 7 pg/ml while a higher dose of 1.5 ng/kg min elicited a supraphysiological increase to 119 +/- 11 pg/ml. Infusion of hG-17 caused a significant increase of the LESP from 19.0 to 25.8 mmHg (p < 0.05, low dose) and from 18.5 mmHg to 23.3 mmHg (p < 0.05, high dose) when compared to the effect of i.v. saline. To exclude effects of augmented acid secretion during hG-17 infusion the experiments were repeated after complete blockade of acid secretion with famotidine 40 mg i.v. After famotidine pretreatment hG-17 caused a similar increase of LESP from 20.1 to 25.9 mmHg (low dose) and from 19.9 to 24.1 mmHg (high dose).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

[Laser lithotripsy of refractory bile duct calculi after failure of extracorporeal shock wave treatment].

UNLABELLED: After failure of extracorporeal shockwave lithotripsy (ESWL) the benefit of further nonsurgical methods for treatment of difficult bile duct stones is undetermined. Endoscopic laserlithotripsy is a promising procedure providing target application of high energy levels. METHOD: Twenty patients (median age: 81 [67-91] years) were referred for laserlithotripsy of 1-8 (median, 2) difficult bile duct stones after failure of 1-4 (median, 3) ESWL sessions. The median diameter of each of the largest stone was 22 (10-48) mm. The laser used was a pulsed rhodamine laser (wavelength: 594 nm) with an automatic cut-out system upon no stone contact. The laser fiber was positioned by means of ERCP under fluoroscopic control or by use of mini-cholangio-scopes. Laserlithotripsy was cholangioscopically performed via the percutaneous transhepatic route in 8 patients because of retrogradely inaccessible bile ducts (n = 5) or because further ERCP was refused (n = 3). All procedures were carried out under intravenous sedation and/or analgesia. RESULTS: Laser lithotripsy and complete removal of fragments was achieved in 19 of the 20 patients after application of 70-25700 (median, 3310) pulses in 1.2 sessions per patient. Median duration of a single session was 70 (15-140) minutes. The procedure failed in one patient with an impacted stone at the cystic duct confluence. Cholangitis could be conservatively managed in 2 cases. No further complication was observed. The 30-day mortality rate was 0 %. CONCLUSION: Endoscopic laserlithotripsy is an effective, a rapid and safe procedure for bile duct stones even after failure of ESWL. The results compare favorably with open surgery, particularly in view of an increased risk in a group of elderly patients.

Aged↗
PubMed1995

Smoking as a risk factor for duodenal ulcer relapse. RUDER Study Group.

This study reports the influence of smoking on the two-year relapse rate of duodenal ulcers under treatment with ranitidine. 1899 patients with a healed duodenal ulcer received 150 mg ranitidine daily for one year, 1671 patients for two years. During this time period 23.4% of smokers relapsed compared with 26.3% of ex-smokers and 18.0% of non-smokers. The difference between smokers and ex-smokers versus non-smokers was statistically significant. There were significantly fewer relapses among smokers who stopped smoking (14.2%) compared with smokers who continued to smoke (25.2%) during maintenance treatment. These results show that continued and past smoking significantly increase the two-year relapse rate of duodenal ulcers during maintenance treatment with ranitidine.

Adult↗
PubMed1994

[MALT lymphoma, stomach carcinoma--role of Helicobacter pylori. Are chances for prevention on the horizon?].

The pathogenesis of gastric carcinoma developing after infection with Helicobacter pylori now seems to be clear. The release of urease, alcohol dehydrogenase, enzymes and cytotoxin on the one hand, and chemotactic factors, PAF and heat-shock proteins on the other trigger chronic inflammation and epithelial metaplasia and dysplasia in the stomach. Under the influence of additional carcinogens, the epithelial changes progress to severe dysplasia and finally carcinoma. As a result of chronic inflammation, MALT lymphomas can also be induced. These can be made to regress by eradicating Hp. The possibility of being able to prevent up to 80% of the carcinomas of the stomach by eradicating Hp holds out good prospects, over the long-term, for the prevention of these tumors. Accurate identification of the patient groups carrying a high risk is now necessary.

Cell Transformation, Neoplastic↗
PubMed1994

Different regulation by pHi and osmolarity of the rabbit ileum brush-border and parietal cell basolateral anion exchanger.

1. The purpose of this study was to look for evidence of a pH-sensitive modifier site on the parietal cell basolateral anion exchanger, determine the pH range in which allosteric regulation takes place, investigate the effect of the osmolarity on internal pH (pHi) dependence and compare it with that of the ileum brush-border anion exchanger. 2. When the pHi in parietal cell basolateral membrane (BLM) vesicles was increased, the rate of Cl(-)-gradient-driven 36Cl- uptake increased from 6.03 +/- 2.24 to 38.09 +/- 3.33 nmol (mg protein)-1 with the steep increase in anion exchange rates occurring within a narrow pH range between pHi 7.0 and 7.5. This was due to allosteric activation by internal OH- and not due to a change in driving force, since the driving force for maximal exchange rates was provided by the outwardly directed Cl- gradient. 3. The pHi dependency curve of parietal cell BLM anion exchange rates was shifted to the left by 0.25 pH units by increasing the osmolarity of the intra- and extravesicular solutions from 300 to 380 mosmol l-1. Thus cell shrinking may activate the parietal cell anion exchanger without a change in pHi and without phosphorylation of the anion exchanger protein. 4. In ileum brush-border membranes, the pHi-dependent increase in the rate of Cl(-)-gradient-driven 36Cl- uptake was more gradual and the half-maximal anion exchange rate was attained at lower pHi (pH 6.5). Increasing the osmolarity from 300 to 500 mosmol l-1 had no effect on pH dependence. 5. We conclude that the parietal cell basolateral and ileum brush-border anion exchangers possess an internal modifier site for allosteric activation by OH-, but the pH range in which allosteric regulation occurs differs between the two exchangers, as does the effect of an increase in osmolarity. Since current evidence suggests that both the parietal cell basolateral and the ileum brush-border anion exchanger are encoded by the AE2 gene, the differences in pHi dependence between the two may be due to alternative splicing, post-transcriptional modification, or the different membrane environment. 6. The pHi range for allosteric activation found in this study would suggest that for both the ileum and the parietal cell anion exchanger, but especially for the latter, a potentiating effect of the allosteric activation and the HCO3- availability occurs within the physiological pHi range and can cause dramatic increases in maximal anion exchange rates with increasing pHi.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1994

[Carbohydrate substitutes: comparative study of intestinal absorption of fructose, sorbitol and xylitol].

BACKGROUND: The carbohydrate substitutes fructose, sorbitol and xylitol are gaining more and more importance in the production of dietary food. But they can provoke gastrointestinal side-effects. In a randomized double blind study the rate of malabsorption of these sugars was compared and the concomitant symptoms were recorded. SUBJECTS AND METHODS: 25 healthy controls received 25 g of each sugar within 3 consecutive days. The intestinal absorption was determined by H2-exhalation tests and the clinical symptoms were recorded. RESULTS: The rate of malabsorption was 84% for sorbitol, 36% for fructose and 12% for xylitol (p < 0.01 for sorbitol versus fructose and xylitol). 57% of the participants with pathological H2-test after sorbitol and 56% after fructose reported symptoms, while all of the 3 malabsorbers of xylitol were symptomatic. CONCLUSIONS: There is an advantage to administering xylitol and fructose with regard to the intestinal absorption and concomitant symptoms as compared with sorbitol. H2-exhalation tests appear to be a reliable diagnostic tool to detect carbohydrate malabsorption and should find broader application in patients suffering from non-specific abdominal complaints.

Adult↗
PubMed1994

Functional characterization of a muscarinic receptor stimulating gastrin release from rabbit antral G-cells in primary culture.

In previous studies carbachol-induced stimulation of gastrin release from antral G-cells in primary culture suggested the presence of muscarinic acetylcholine receptors on this cell type. Therefore, we attempted to pharmacologically characterize the muscarinic acetylcholine receptor subtype involved. Enzymatically isolated rabbit antral mucosal cells (0.8% G-cells) were separated by counterflow elutriation yielding a fraction (1.7% G-cells) that was placed in culture on collagen-coated well plates. After 24-36 h of culture 13.0 +/- 2.4% of total adherent cells were immunoreactive for gastrin as shown by immunocytochemical staining using the avidin-biotin complex method. In this preparation basal gastrin release ranged from 3.3 +/- 0.3 to 4.1 +/- 0.3% of total cellular content. Maximal gastrin release in response to the acetylcholine receptor agonist carbachol (10(-4) M) or the selective muscarinic receptor agonist arecaidine propargyl ester (10(-4) M) was 8.5 +/- 0.4% and 7.6 +/- 0.4% of total cellular content, respectively. The EC50 values were 3.7 +/- 0.5 x 10(-6) M carbachol and 1.8 +/- 0.4 x 10(-6) M arecaidine propargyl ester. At a concentration of 10(-6) M the non-selective muscarinic receptor antagonist atropine and the muscarinic M3 receptor preferring antagonist hexahydro-sila-difenidol (HHSiD; M3 > or = M1 > M2) completely inhibited gastrin release in response to carbachol (Ki values: 52 x 10(-9) M atropine and 29 x 10(-9) M HHSiD) and arecaidine propargyl ester (Ki values: 11 x 10(-9) M atropine and 13 x 10(-9) M HHSiD).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

[Substitution of factor XIII concentrate in treatment refractory ulcerative colitis. A prospective pilot study].

BACKGROUND: Severe acute inflammation in ulcerative colitis is often associated with major intestinal blood loss. Studies on hemostasis present a deficiency of F XIII which is important for clot formation and wound healing. PATIENTS AND METHODS: A total of ten patients had been treated with 5-aminosalicylic-acid and corticosteroids consequently for three weeks. Thereafter a clinical improvement did not occur, the colitis activity index (CAI) and the endoscopic score (ES) remained elevated (9.9 +/- 1.5 points and 8.9 +/- 2.3 points, respectively). Because of this therapy-resistant active stage of disease in an open and prospective pilot trial F XIII concentrate (1,250 IU, Fibrogammin HS, Behringwerke, Germany) was additionally administered intravenously for ten days. RESULTS: The additional substitution therapy resulted in a significant improvement of complaints, the stool frequency decreased from 9 +/- 4.1 to 2.4 +/- 1.5 (p < 0.001). Both, the clinical activity index (2.8 +/- 1.6; p < 0.0001, vs day 0) and the endoscopic score (4.4 +/- 2.2; p < 0.005, vs day 0) declined significantly during the F XIII substitution. The F XIII activity was markedly reduced initially (46.1 +/- 17.4%) and showed a significant increase after the substitution (171 +/- 41.7%; p < 0.001). CONCLUSION: The results may suggest that substitution therapy with F XIII concentrate can be beneficial in patients with therapy-resistant active stage of ulcerative colitis and proven F XIII deficiency. To verify this preliminary results, controlled clinical trials will have to be performed.

Acute Disease↗
PubMed1994

Exendin-4 and exendin-(9-39)NH2: agonist and antagonist, respectively, at the rat parietal cell receptor for glucagon-like peptide-1-(7-36)NH2.

Exendin-4 is a novel peptide from Heloderma suspectum venom which is 53% homologous with glucagon-like peptide-1 GLP-1-(7-36)NH2, a stimulant of cAMP-dependent H+ production in rat parietal cells. It was the aim of the present study to determine whether this effect of GLP-1-(7-36)NH2 is shared by exendin-4, and whether the responses to either peptide are blocked by exendin-(9-39)NH2, a competitive specific exendin receptor antagonist. In enriched rat parietal cells H+ production was measured indirectly by [14C]aminopyrine accumulation. cAMP production was determined by radioimmunoassay. [125I]GLP-1-(7-36)NH2 was prepared using chloramine T followed by high pressure liquid chromatography (HPLC) purification. Exendin-4 (10(-12) - 10(-8) M) stimulated [14C]aminopyrine accumulation in a concentration-dependent manner (EC50 = 7.6 x 10(-11) M). At the maximally effective concentration (10(-9) M) exendin-4 was as effective as GLP-1-(7-36)NH2 reaching 70-80% of the response to 10(-4) M histamine. Likewise, exendin-4 (10(-11) - 10(-7) M) stimulated parietal cell cAMP production up to 2.8-fold. Maximal stimulation by exendin-4 of [14C]aminopyrine accumulation was not affected by ranitidine (10(-4) M), but was concentration-dependently reduced by exendin-(9-39)NH2 (10(-11) - 10(-7) M). At the maximal concentration, exendin-(9-39)NH2 completely abolished the responses to 10(-9) M exendin-4 and to 10(-9) M GLP-1-(7-36)NH2 while not altering stimulation by 10(-4) M histamine. Binding of [125I]GLP-1-(7-36)NH2 to enriched parietal cells was displaced by exendin-4 (Ki = 4.6 x 10(-10) M) as well as by exendin-(9-39)NH2 (Ki = 4.0 x 10(-9) M).(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopyrine↗
PubMed1994

Release of bombesin-like immunoreactivity from synaptosomal membranes isolated from the rat ileum.

In the enteric nervous system, direct effects on peptidergic neurotransmitter release are difficult to assess since the neuronal network predisposes to numerous interactions between the various transmitter systems. The aim of the present study was to examine the release of bombesin-like immunoreactivity from isolated nerve synapses of the enteric nervous system. Enriched synaptosomal fractions were obtained by using homogenized tissue from rat ileum, which was subjected to various steps of differential and sucrose density centrifugation. Specific binding of [3H]saxitoxin served as a marker for neuronal membranes. For comparison, the content of bombesin-like immunoreactivity was determined. Both the enriched synaptosomal fraction (mitochondrial fraction II or P2) and the purified synaptosomal fraction (F2), obtained after discontinuous sucrose density centrifugation, showed substantial enrichment of the neuronal marker [3H]saxitoxin and bombesin-like immunoreactivity. The basal release of bombesin-like immunoreactivity was 52 +/- 17 pg/mg (100%). KCl-evoked depolarization (65 mM) significantly stimulated the release of bombesin-like immunoreactivity to 142.2% (P < 0.05, n = 17). The release was abolished in Ca(2+)-free medium. Stimulation of the release of bombesin-like immunoreactivity was also observed in the presence of the Ca2+ ionophore A-23187 (10(-6) M: 129%, P < 0.05, n = 17), supporting the role of Ca2+ in the release process. Cholinergic stimulation with carbachol elicited a significant dose-dependent release of bombesin-like immunoreactivity (10(-8) M: 106%, 10(-7) M: 175%, P < 0.05, 10(-6) M: 156%, P < 0.05, 10(-5) M: 115%, n = 14), which was reduced by atropine (10(-6) M: 99%, P < 0.01, n = 14). The basal value was 67 +/- 9 pg/mg (100%). The different effects of the muscarinic M1 receptor antagonist pirenzepine, which stimulated release of bombesin-like immunoreactivity in combination with carbachol 10(-6) M (10(-6) M: 123%, n = 10), and of the muscarinic M2 receptor antagonist AFDX 116, which attenuated release of bombesin-like immunoreactivity evoked by carbachol (10(-5) M: 66%, P < 0.01, 10(-6) M: 88%, n = 10), strongly suggest modulation of the release of bombesin-like immunoreactivity at the presynaptic receptor site through an excitatory muscarinic M2 receptor. The basal value was 46 +/- 9 pg/mg (100%). In summary, bombesin-like immunoreactivity can be released from these synaptosomes by both depolarization with KCl in a Ca(2+)-dependent manner and by cholinergic stimulation. The synaptosomes of intrinsic nerves of the gut offer an approach to study the release of neuropeptides and neurotransmitters at the subcellular level independent of the ganglionic network.

Animals↗