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Biomedical subjects

M Wienbeck

Publications and source records attributed to M Wienbeck.

At least 127 records · Page 7Linked to original sources
PubMed1987

[Effect of L-tryptophan on fasting intestinal motility and intestinal transit time in the human].

Since previous experiments in dogs suggested L-tryptophan to disturb the migrating motor complex (MMC) we set out to study its effects in man. In six healthy volunteers intraduodenal instillation of 50 mmol L-tryptophan did not disrupt the interdigestive motility pattern. In comparison to saline L-tryptophan caused a brief and local increase of motor activity in the upper small bowel. There was no change in small bowel transit time. The oral intake of 560 kcal liquid formula diet produced a typical digestive pattern for 160-209 min. The increase and the maximum of serum gastrin levels did not correspond to the changes of motor activity.

Adolescent↗
PubMed1987

Ricinoleic acid and loperamide have opposite motor effects in the small and large intestine of the cat.

The actions of laxatives and antidiarrheal agents in the gut are incompletely understood. Therefore, the effects of Na ricinoleate 10(-4)-10(-2) g/kg b. w. and of loperamide 10(-4) g/kg b. w. on myoelectric activity and marker propulsion were studied in the small and large intestine of 7 unanesthetized cats. Intraduodenal application of ricinoleate briefly increased and then decreased spike activity in the small intestine; marker transit was delayed (92 +/- 18 min vs. 55 +/- 14 min in controls). Ricinoleate also initiated spike complexes of 10-215 sec duration. Transit from the right to the left colon was sometimes accelerated and sometimes delayed. The number of uncoupled slow waves was increased to 278% of control. Loperamide accelerated small intestinal transit to 17 +/- 6 min and markedly delayed it in the colon. At the same time it caused a strong and prolonged rise in colonic spike activity. When ricinoleate and loperamide were given together, their effects almost compensated for each other. The resulting net effect was similar to the data in the control experiments. It is concluded that laxatives and antidiarrheal agents alter not only transit, but also myoelectric activity in the small and large intestine. The effects are largely in opposite direction. Loperamide may, therefore, antagonize motor effects of ricinoleate in the gut.

Animals↗
PubMed1987

[Motility and peptic ulcer--possible pathogenetic relations].

The most important causes of peptic ulcers are increased gastric acid secretion, impaired mucosal circulation and damages to the mucosa. In contrast, motility plays only a minor role. The following motility disturbances are discussed in peptic ulcers: 1. Impaired gastric emptying may favor the development of gastric ulceration, if it is grossly delayed, and that of duodenal ulceration, if it is inappropriately accelerated. 2. Disturbances of duodenal motility in the fasted state may disturb bicarbonate secretion and, thus, become theoretically ulcerogenic. 3. Duodenogastric reflux has been discussed as a cause of gastric ulceration for a long time; yet, the proof is still missing. 4. According to own studies gastric ulcer is frequently accompanied by morphological and functional changes in the antrum; the cause-effect relationship, however, has yet to be elucidated.

Animals↗
PubMed1986

[Different healing tendencies of reflux esophagitis following omeprazole and ranitidine. Results of a German-Austrian-Swiss multicenter study].

The effectiveness of a single, morning oral dose of 40 mg omeprazole or a twice daily oral dose of 150 mg ranitidine was compared in a randomized endoscopically controlled double-blind trial at 37 clinics in Austria, Germany and Switzerland. A total of 178 out-patients in stages I-IVa (after Savary and Miller) were entered into the trial: 78 in stage I, 60 in stage II, 27 in stage III, and in 13 in stage IVa. As early as at the end of the third treatment week there was a significantly higher rate of complete healing or reduction into a lower stage with omeprazole than ranitidine (85% vs 67%; P less than 0.02). After six treatment weeks, healing tendency after omeprazole compared with ranitidine was 85% vs 45% (P less than 0.04). Omeprazole also brought earlier improvement in symptoms. The difference was statistically significant for heartburn (pyrosis): P less than 0.01. Both drugs were equally well tolerated and there were no clinically significant side-effects. This is the first demonstration that the ATPase inhibitor omeprazole is superior to the H2-receptor antagonist ranitidine in the treatment of reflux oesophagitis.

Administration, Oral↗
PubMed1986

[2 or 1 daily doses of ranitidine in the treatment of reflux esophagitis].

In a randomized multicentre study 96 patients with mild to moderate types of reflux esophagitis (stages I and II according to Savary-Miller) the effect of 150 mg ranitidine b.i.d. (49 patients) was compared to that of 300 mg ranitidine nocte (47 patients). In both patient groups similar healing rates were observed. 81.6% and 74.5%, respectively, of the patients with esophagitis healed within 6 weeks, and 95.9% and 93.6%, respectively, within 12 weeks. Reflux symptoms disappeared in both treatment groups in 91.8% and 80.9%, respectively, within 6 weeks, and 98.0% and 100%, respectively, within 12 weeks. Drug safety was good. Thus, in mild to moderate types of reflux esophagitis treatment with ranitidine can be reduced to one single dose of 300 mg at night.

Adult↗
PubMed1986

Effects of an enkephalin analog on motility of the small and large intestine in the cat.

In order to study the effects of naturally occurring opioids on intestinal motility we exposed the unanesthetized cat to different doses of methionine (Met)-enkephalin analog DAMME. DAMME 10(-10) and 10(-9) M/kg body weight inhibited spike activity in the small intestine 20-50 min after injection, whereas in the colon doses as low as 10(-11) M/kg stimulated spiking. Transit of a radiopaque marker infused into duodenal and cecal catheters was delayed both in the small and large bowel. The enkephalin effect was inhibited by the opiate antagonist naloxone 10(-8) and 10(-7) M/kg in the colon, but only at 10(-7) M/kg in the small intestine. Atropine suppressed the enkephalin effect in the small, but not in the large bowel. DAMME caused central nervous side effects. It is concluded that the Met-enkephalin analog suppresses myoelectrical activity in the small intestine probably via cholinergic nervous pathways, and it stimulates spiking and segmenting contractions in the colon probably via a myogenic action. Opiate antagonists may be useful in the treatment of constipation if endogenous opioids are involved.

Animals↗
PubMed1986

[Familial dysphagia].

The etiology of achalasia and diffuse esophageal spasm remains unknown. We report on two families (father/son, mother/son) with achalasia and esophageal spasm, respectively, who were examined by radiology, endoscopy and manometry. One patient (mother) died from aspiration pneumonia. These observations support the hypothesis of a genetic trait in some cases of esophageal motility disorders. In addition, the coincidence of familial achalasia and esophageal spasm is in support of a close relationship of both diseases. Achalasia is a potentially letal disorder.

Adult↗
PubMed1985

[Intramural pseudodiverticulosis of the esophagus. Clinical aspects, morphologic changes and functional disorders].

Oesophageal intramural pseudodiverticulosis, a rare benign disease with as yet unexplained aetiology, was observed in 4 patients during the course of 2 years. The main symptom is dysphagia. Radiographic and endoscopically detectable diverticula or diverticular orifices are pathognomonic. A prolongation in the duration of oesophageal contractions is the main manometric finding. At autopsy, a reduction in the number of oesophageal intramural ganglion cells was seen in one case. A prolonged pressure-effect on the oesophageal wall could be the cause of the wall pouches.

Adult↗
PubMed1985

Effects of morphine and atropine on motility and transit in the human ileum.

We examined motility of the ileocecal region, pressures at the ileocecal sphincter, and ileal flow after therapeutic doses of morphine and atropine. Using a factorial design in two cells of 8 (2(3] subjects, drugs were given during fasting and postcibally. Morphine (100 micrograms/kg body wt as a bolus intravenously) and atropine (7 micrograms/kg body wt as a bolus) stimulated migrating bursts of phasic activity (similar to phase III of the migrating motor complex). Morphine initially stimulated ileal flow, but atropine could not be shown to have this effect. Atropine reduced markedly the occurrence of sporadic pressure waves in the ileum, but morphine did not. Whereas atropine delayed mouth-to-ileum transit of polyethylene glycol, given in a mixed meal, morphine did not. Naloxone, in the dosage used (40 micrograms/kg body wt as a bolus, followed by 10 micrograms/kg body wt X h) had no independent effects on motility or flow, but did blunt the stimulatory effects of morphine and atropine on migrating motor complexes. We could not demonstrate an effect of any drug on the transit of lactulose from terminal ileum to cecum. Neither morphine nor atropine had impressive effects on tone at the ileocecal sphincter. These observations, while not specifying the mechanisms for constipation after opiates or anticholinergics, highlight the complexities of small bowel transit in humans and point out that the antidiarrheal effects of drugs are probably multifactorial.

Adult↗
PubMed1985

Comparative radiological and morphological study of human pancreas. Pancreatitis like changes in postmortem ductograms and their morphological pattern. Possible implication for ERCP.

A postmortem study by ductography and histology was performed on 69 human pancreata with no clinical or histological signs of chronic pancreatitis. The ductograms, supplemented by five postmortem ductograms of chronic pancreatitis, were independently evaluated by six clinicians, skilled in ERCP; the degree of alteration was estimated by simple rating, forced choice rating, and by determination of the grade of chronic pancreatitis, Histologically, the amount of intraductal epithelial proliferation, periductal, intralobular and perilobular fibrosis, intraductal protein plugs, and fat necrosis was determined by semiquantitative methods. The six ductographical evaluations significantly differed in the level of their data, but corresponded in the range of distribution. All evaluations were correct regarding judgement of ductograms from patients with chronic pancreatitis. Ductograms of patients without chronic pancreatitis, however, were also frequently classified as chronic pancreatitis; overall 81% (minimal 37%, moderate 33%, severe 11%). This high level of false positive diagnosis indicates the frequency of pancreatitis like lesions in the main duct and its side branches in patients without chronic pancreatitis. Ductal lesions were significantly correlated with perilobular fibrosis. This finding favours the assumption, that in the non-inflamed pancreas, perilobular fibrosis plays a key-role in the development of ductal alterations, as in chronic pancreatitis. Perilobular fibrosis may result from intralobular inflammation caused by age-dependent intraductal epithelial hyperplasia.

Adult↗