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Biomedical subjects

W P Fritsch

Publications and source records attributed to W P Fritsch.

At least 37 records · Page 2Linked to original sources
PubMed1983

[Treatment of duodenal ulcer with synthetic depot secretin - a double-blind study].

63 inpatients with duodenal ulcer disease were treated with either depot-secretin or placebo. Two different secretin-regimens were used. In group I 18 patients were given secretin twice daily. 11 ulcers from a total of 19 ulcers healed within 3 weeks. In group II 23 patients were given secretin once daily. 21 out of 28 ulcers healed within 3 weeks. In the placebo-treated group 24 ulcers were observed in 22 patients. Of these 15 healed within 3 weeks. There was no statistical difference in the healing rate between the 3 groups. However, depot-secretin significantly improved typical symptoms. Analgetics were used less frequently. Serious side effects did not occur.

Adult↗
PubMed1982

[Real-time sonography of upper abdominal arteries and veins (author's transl)].

Improved resolution of new real time sonographic equipment permits demonstration and demarcation of vascular structures which could not be differentiated formerly. Successful differentiation frequency of upper abdominal vessels and establishment of optimal transducer position were investigated prospectively in 100 patients undergoing sonographic upper abdominal assessment. Aorta, inferior vena cava and their branches were identified in a high percentage. Portal vein contributaries could be demarcated in over 70%. Real-time sonography enables rapid assessment of vascular structures. Pulse and respiration dependent variations of calibre are a valuable means for differentiation.

Abdomen↗
PubMed1982

The inhibition of vagal stimulated acid secretion by pirenzepine and cimetidine.

H2-receptor-antagonists inhibit pentagastrin-stimulated acid secretion for a longer period than basal secretion. Anticholinergic drugs and pirenzepine are less effective and act differently by reduction of volume. Acid concentration is reduced to 95% by cimetidine compared to 20% by atropine and pirenzepine. By increasing electrical vagal stimulation there is a decreasing effect of cimetidine. In contrast, atropine and pirenzepine inhibit vagally transmitted acid secretion by about 45%, even when vagally stimulated acid secretion amounts to more than 50% of the pentagastrin-stimulated secretion. These results support the hypothesis of histaminergic and cholinergic receptors in man.

Atropine↗
PubMed1982

The effect of a 100 mg pirenzepine--treatment on acid secretion and serum gastrin.

50 mg pirenzepine inhibit basal acid secretion by 39.9% and peptone-stimulated acid output by 21.3%. The percentage of inhibition is nearly doubled if the same dose is given after a treatment with 50 mg pirenzepine twice daily for 3 to 7 days. No acute effect on serum gastrin levels can be demonstrated by a single dose of pirenzepine. After pretreatment only a small increase of basal gastrin levels is observed, serum gastrin does not change during stimulation. On the bases of these results the effect on ulcer healing by high doses of pirenzepine is probably due to a much more pronounced acid inhibition. One reason for stronger inhibition of acid secretion after pretreatment with pirenzepine is probably accumulation of the drug, other reasons may be distribution space or receptor binding. The effect of anticholinergic drugs on serum gastrin concentrations is probably dose-dependent.

Benzodiazepinones↗
PubMed1982

[Acid secretion and gastrin release following stimulation with intragastric instillation of a peptone solution in healthy probands and patients with duodenal ulcer].

In 19 DU-patients and in 15 control subjects acid secretion tests were performed by continuous aspiration or by intragastric titration. Pentagastrin (6 micrograms/kg subcutaneously) or a 20% peptone solution (intragastric instillation) were used for stimulation. In 10 control subjects pentagastrin stimulated acid secretion was within the normal range, hypersecretion (greater than 32 mmol/h) was found in the other 5. 14 DU-patients showed hypersecretion, 5 had normal acid secretion. In contrast to these findings intragastric peptone stimulation caused a very uniform acid secretion within each group. Based on these results ulcer patients and healthy controls could be discriminated more exactly. Acid secretion and serum gastrin concentration were significantly higher in DU patients than in controls. There was a significant correlation between maximal gastrin concentrations and peak acid output after peptone stimulation.

Duodenal Ulcer↗
PubMed1981

[Acid secretion and serum gastrin during acute and chronic treatment with pirenzepine in duodenal ulcer (author's transl)].

In 8 outpatients with duodenal ulcer the effect of a single dose of 50 mg pirenzepine is compared to a 3-7 days treatment with 2x50 mg. Basal and peptone-stimulated acid output is measured. A single dose of 50 mg pirenzepine reduced basal acid output by 39,9% and the stimulated acid secretion by 21,3%. Treatment for 3-7 days with 2x50 mg pirenzepine is significantly more effective. Basal acid output is reduced by 75,1% and stimulated acid output by 54,0%. No acid inhibition can be demonstrated 12 hours after the last drug administration. Basal serum gastrin levels are little but significantly increased after chronic treatment.

Administration, Oral↗
PubMed1980

Evidence for the secretion of gastrin into human gastric juice.

Provided the intragastric pH is greater than 6 and the collected gastric juice is boiled and neutralised immediately, considerable amounts of gastrin-like immunoreactivity can be found in human gastric juice. Characterisation according to size and charge reveals that nearly all the gastrin-like immunoreactivity is similar to gastrin 1-17. Direct stimulation of the G-cells with protein solution is followed by a significant and simultaneous increase of acid secretion, serum gastrin, and gastrin output into the lumen of the stomach in control subjects and patients with duodenal ulcer.

Chromatography, Gel↗
PubMed1980

Effects of cimetidine and pirenzepine on peroperative electrical vagal stimulation of gastric acid secretion.

Atropine and an eightfold greater amount of pirenzepine inhibit pentagastrin-stimulated secretion to nearly the same extent (70-75%). Neither drug influences acid concentrations markedly (18%). Atropine and pirenzepine decrease the potassium concentration of gastric juice. By increasing electrical vagal stimulation the inhibitory effect of cimetidine decreases. In contrast, inhibition of vagally stimulated secretion by pirenzepine or by atropine averages 45%, when vagally stimulated secretion amounts to more than 50% of the pentagastrin-stimulated secretion. Thus pirenzepine inhibits gastric secretion similarly to atropine. These results support the hypothesis of a histamine and a cholinergic receptor.

Adult↗
PubMed1980

[Comparison of the effects of natural and synthetic secretin on the exocrine secretion of the human pancreas (author's transl)].

In 16 healthy male subjects the effects of natural and synthetic secretin on the function of the exocrine pancreas were compared. Following; stimulation with secretin in all cases pancreozymin was injected to ascertain normal pancreatic secretory capacity. The methods applied corresponded to those used in the multicenter study of the European Pancreatic Club. No significant differences were found between the results concerning volume of secretion, maximal bicarbonate concentration, maximal bicarbonate output and enzyme secretion rates after stimulation with natural and synthetic secretin, respectively. It is concluded that the synthetic peptide can be utilized in the same way as the natural product in the secretin-pancreozymin-test.

Bicarbonates↗
PubMed1980

[The significance of human gastric juice gastrin to acid secretion (author's transl)].

Gastrin 1--17 protected against physiological proteolysis does not change gastric acid secretion and serum gastrin level even if present in the duodenal and gastric lumen in excessive amounts. Consequently gastric juice gastrin has no local effect on the parietal cell. There is no measurable resorption of gastrin from the gastric or duodenal lumen. Gastrin 1--17 does not liberate endogenous gastrin from the antral and duodenal mucosa. Thus, an indirect systemic influence of gastric juice gastrin on the function of the parietal cell can be excluded. Gastric juice gastrin seems to be a waste-product of a bidirectional G-cell secretion. Gel filtration and starch block electrophoresis revealed considerable amounts of immunoreactive material in the duodenal perfusate resembling gastrin 1--34. Thus, the duodenal G-cells seem to liberate gastrin into the duodenal lumen.

Duodenal Ulcer↗
PubMed1980

[Evidence for the secretion of gastrin into the duodenal lumen of man].

In six healthy male subjects the duodenum was perfused with phosphate buffer and peptone respectively via a double balloon tube. During peptone perfusion secretion of gastrin into the duodenal lumen and serum gastrin rose simultaneously and significantly compared with buffer control. There was a significant but delayed increase of gastric acid secretion. 60 % of the gastrinlike immunoreactivity in duodenal perfusates corresponded to gastrin 1-34 and 40 % to gastrin 1-17 when separated by starch gel electrophoresis and gel filtration.

Duodenum↗
PubMed1980

[Secretory mechanism of intragastric gastrin in man].

Gastric acid secretion and gastrin-like immunoreactivity in serum and gastric juice of six healthy subjects were measured during an increasing intravenous administration of pentagastrin and compared with basal values obtained during intravenous infusion of 0.9% NaCl. Gastric acid secretion and gastrin-like immunoreactivity in the serum increased significantly during infusion of pentagastrin. Gastrin-like immunoreactivity released into the gastric lumen was unchanged from the NaCl control. This is a further evidence for direct secretion of gastrin into the lumen of the stomach from antral G-cells.

Gastric Juice↗