[Endoscopic insertion of endoprostheses in benign bile duct calculi. Description of 4 cases].
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Aged↗
Biomedical subjects
F Halter
Publications and source records attributed to F Halter.
Structure and function of gastric corpus mucosa in suckling rats after treatment with 16,16-dimethyl prostaglandin E2.
Suckling rats were treated every 8 h by intragastric instillation of 16,16-dimethyl prostaglandin E2 (PG) from postnatal day 7 to 11. As compared to saline control treatment, PG increased the thickness of antral and corpus mucosa, the volume density of parietal cells, the mean individual parietal cell volume and pentagastrin-stimulated acid secretion at the end of the treatment. Plasma gastrin and corticosterone levels were depressed by PG while plasma thyroxine levels were unchanged. These structural and functional changes suggest PG-induced accelerated maturation of gastric mucosa.
16,16-Dimethylprostaglandin E2↗
Indomethacin and turnover of gastric mucosal cells in the rat.
Mucosal morphology and the balance between cell loss and cell renewal were analyzed during treatment with a non-ulcerative dose of indomethacin. All rats were treated twice daily by subcutaneous injection of 2 mg/kg indomethacin or the solvent. The following parameters were assessed: cell proliferation on day 3 (determination of in vitro [3H]thymidine incorporation), cell migration on days 1 and 3 (autoradiography), cell shedding on days 7 and 14 (measurement of the remaining DNA-bound mucosal radioactivity after in vivo labeling with [3H]thymidine prior to treatment), mucosal morphology on day 14 (light microscopy), ex vivo mucosal prostaglandin E2 on day 14, and serum gastrin on days 0, 7, and 14. Indomethacin treatment had no effect on serum gastrin levels but reduced mucosal prostaglandin E2. Indomethacin produced a significant increase of [3H]thymidine incorporation, cell migration, and loss of mucosal DNA-bound radioactivity in the corpus and, to a lesser degree, in the antrum. Morphologically, this led to a hyperplasia of parietal cells (+15%, P less than 0.05) and chief cells (+45%, P less than 0.01) in the corpus, but antral morphology remained unchanged. We conclude that indomethacin stimulates the turnover of gastric mucosal cells. In the corpus, but not in the antrum, proliferation exceeds shedding, thus leading to increased mucosal volume.
Animals↗
Effect of acid inhibition on the growth of parietal cells.
Studies in the rat have shown that prolonged inhibition of acid secretion by high doses of a histamine H2 antagonist is followed by a 20-30% increase in the number of parietal cells, and that this is paralleled by an augmentation of the maximum acid output. A similar effect has been shown after prolonged acid neutralization with high doses of an antacid. These trophic effects are not unexpected. An increase in gastric pH is followed by gastrin release, and the parietal cell mass may be augmented by repeated exogenous administration of gastrin or by endogenous hypergastrinaemia following surgery. To further evaluate whether a direct correlation exists between the magnitude of drug-induced hypergastrinaemia and parietal cell hyperplasia, rats were treated for 24 days with two acid inhibitors which differ markedly in the degree of acid inhibition and acute or chronic gastrin release. Six animals each were treated with either omeprazole (40 mumol/kg once daily), or atropine (3 mg/kg twice daily), or omeprazole combined with atropine or with placebo. On day 24, plasma gastrin was elevated more than 10-fold in both groups of rats treated with omeprazole but not in animals given atropine alone. As compared to placebo treatment, total parietal cell volume was significantly higher in animals treated with atropine (102 +/- 9 mm3 versus 140 +/- 18 mm3), but was unchanged in the other two groups. These studies demonstrate that marked prolonged drug-induced hypergastrinaemia does not necessarily exert trophic effects on parietal cells. Furthermore, the finding that omeprazole abolishes the effect of atropine suggests that omeprazole interferes with trophic actions on parietal cells.
Animals↗
Effects of secretin antibody on gastric acid inhibition and pancreatic bicarbonate stimulation by acidified liver extract meal in dogs.
Duodenal acidification is known to inhibit gastric H+ secretion while stimulating pancreatic HCO-3 secretion, but the mechanisms of these effects have not been fully explained. This study was designed to determine the role of endogenous and exogenous secretin in gastric inhibition and pancreatic stimulation by an acidified liver extract (LE) meal in conscious dogs prepared with chronic gastric and pancreatic fistulas pretreated with normal serum (control) or anti-secretin serum. In control tests, plasma gastrin and gastric H+ secretion showed a marked rise with LE meals at pH ranging from 7.0 to 4.0, but significantly declined at pH 3.0 and 2.0. Plasma secretin and pancreatic secretion started to rise with LE meals at pHs below 4.5, and both reached peaks at pH 2.0. Exogenous secretin infused at graded doses suppressed plasma gastrin and gastric H+ responses to LE meals at doses of 1.0 and 2.0 U/kg-h, but increased, dose-dependently, plasma secretin and pancreatic HCO-3 starting with a dose of 0.03 U/kg-h. Following the administration of anti-secretin serum, the effects of exogenous secretin on plasma gastrin and secretin levels as well as on gastric and pancreatic secretion were almost completely abolished. The increase in plasma secretin and pancreatic HCO-3 responses to LE meals at pH below 4.5 were also abolished by anti-secretin serum, but the suppression of plasma gastrin level and the inhibition of gastric H+ responses to LE meals at lower pH (3.0 and 2.0) remained virtually unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
[Endoscopic insertion of endoprostheses in malignant extrahepatic bile duct stenoses].
In the vast majority of patients with malignant biliary strictures endoscopic insertion of biliary endoprostheses leads to good palliation with decline of the jaundice and disappearence of the pruritus. The prostheses are positioned immediately after diagnostic endoscopic retrograde cholangiopancreatography, thus causing only minor additional discomfort for the patients. The insertion technique is difficult, but success rates between 70 and 90% are achieved by experienced endoscopists. Complications occur in 10 to 20% and mortality is 2-3%. Thus, endoscopically inserted endoprostheses have become a good alternative to the percutaneous transhepatic procedure and in many cases even to palliative surgical biliary drainage.
Aged↗
[Psychosocial adaptation with an artificial intestinal outlet].
A total of 1625 patients with colostomy, ileostomy or urostomy, including all members of the Swiss ILCO Association, received a questionnaire concerning their medical, social, family and personal situation. 948 questionnaires were analyzed. The mean age was 64 and the time since operation 6 years. 60% regarded their postoperative instruction in stoma care as adequate, but 32% were unhappy with the preoperative information. The transstomal colonic irrigation technique was still unknown to 21% of the colostomy patients and was utilized by only 32%. One year after the operation 69% of the patients with colostomy, 83% with ileostomy and 59% with urostomy in the under-62 age group were fully reintegrated in their professions. Acceptance of the stoma by family and friends was good and there were no major difficulties in practising sports and other hobbies. Sexuality proved to be the most seriously affected aspect of their personal lives, as 33% male and 13% female patients reported major problems.
Adaptation, Psychological↗
In vitro tests overestimate in vivo neutralizing capacity of antacids in presence of food.
The neutralizing capacity of two antacids (Alucol = A, Syntrogel = S), differing both in their composition and theoretical neutralizing capacity, was evaluated in vitro and in vivo. In vitro at pH 3.5, 1 ml of A or S neutralizes 3.9 and 1.6 meq of acid, respectively, in an aqueous solution. When tested in vivo in the absence of food during near maximal acid secretion, induced by impromidine, 60 ml of either A or S reduced the 4-hr mean H+ activity by 83% and 65%, respectively. In contrast, the reduction of the 12-hr H+ activity observed after repeated administration of 30-60 ml of A or S at the end of the postprandial hour failed to reach significance with both preparations. This suggests that interaction with food produces a considerable loss of in vivo antacid neutralizing capacity, not quantitatively predictable from in vitro tests.
Adult↗
Effects of pinaverium bromide and verapamil on the motility of the rat isolated colon.
Pinaverium bromide was 30 times less potent than verapamil in inhibiting intraluminal pressure responses of in vitro rat colonic segments to barium chloride, acetylcholine, FK 33-824 or field stimulation. The inhibitory effects of both verapamil and pinaverium bromide on the pressure responses to field stimulation were antagonized similarly by exogenous calcium administration. These results support the concept that pinaverium bromide acts on calcium channels in the smooth muscle cell membrane.
Acetylcholine↗
Influence of 16,16-dimethyl prostaglandin E2 on morphology and brush border enzymes of small-bowel mucosa. Differences in reactivity between adult and suckling rats.
High doses of 16,16-dimethyl prostaglandin E2 (dmPGE) are trophic to the small bowel of adult and suckling rats. In suckling rats this effect is paralleled by an increase in brush border enzyme activities, possibly indicating accelerated mucosal maturation. To investigate the possible physiological significance of this phenomenon, we examined whether this induction of intestinal enzyme activities can be reproduced in adult rats and whether cell growth and enzyme activity might be suppressed by indomethacin. Treatment twice daily for 2 weeks with 100 micrograms/kg dmPGE by intragastric instillation increased villus length in the proximal and distal small bowel by 36% and 40%, respectively, while 2 mg/kg indomethacin by subcutaneous injection had no effect. Maltase, trehalase, lactase, and sucrase activities were unchanged after dmPGE or indomethacin. [3H]-thymidine incorporation into DNA was not significantly influenced for up to 24 h after a single dose of both 100 micrograms/kg PGE intragastrically or 10 mg/kg indomethacin subcutaneously. These studies confirm that in adult rats large doses of 16,16-dm PGE2 increase the volume of the small-bowel mucosa. In contrast to the situation in suckling rats, the activity of hydrolytic brush border enzymes is not increased. There is thus no evidence that endogenous prostaglandins are trophic or influence brush border enzymes in the adult rat.
16,16-Dimethylprostaglandin E2↗
[Modification of the growth of the gastric mucosa by drugs].
Over the last two decades it has become apparent that various drugs influence growth of gastric mucosa. For example, non-steroidal anti-inflammatory drugs increase cell shedding, which is, in rats at least, overcompensated by stimulation of cell proliferation during long-term treatment. Hyperplasia of parietal and other gastric epithelial cells has been observed in rats treated with many different ulcer drugs. Of special interest are alterations and sometimes neoplasms of gastric mucosa induced by long-term administration of very high doses of novel inhibitors of acid secretion. Some of these tumours are probably the consequence of massive hypergastrinaemia due to alkaline gastric pH and consequent lack of inhibition of gastrin release. In man the increase of gastrin is less marked even after administration of omeprazole, the most potent inhibitor of acid secretion known. Extrapolation of results from animal experiments to the situation of patients with ulcer disease is therefore questionable. However, it cannot be ruled out that total inhibition of acid secretion for a very long period could cause proliferation of gastric endocrine cells, since such tumours occur in endogenous hypergastrinaemia in patients with pernicious anaemia or Zollinger-Ellison syndrome.
Animals↗
Cyclooxygenase inhibitors affect Met-enkephalin- and acetylcholine-stimulated motility of the isolated rat colon.
Endogenous prostaglandins have been shown to modify the contractile activity of the intestinal muscle. In this study, the effects of the cyclooxygenase inhibitors phenylbutazone, diclofenac, indomethacin, acetylsalicyclic acid (ASA) and salicyclic acid (SA) on the motility of the Met-enkephalin- (FK) and acetylcholine- (ACh) stimulated isolated rat colon were observed. Intraluminal pressure changes were measured by perfusion manometry in organ preparations maintained in a standard organ bath. FK and ACh dose-dependently increased intraluminal tonic pressure with a response of 42 +/- 0.6 arbitrary units (mean +/- S.E., n = 6) at 10(-6) M FK and of 96.8 +/- 8.6 arbitrary units at 10(-4) M ACh. Oral pretreatment with ASA (300 mg/kg b.i.d. for 3 days and 1 h before removal of the colon) suppressed the stimulatory effect of FK and significantly reduced ACh stimulation of colonic tone. A similar effect was observed when ASA alone was added to the nutrient. Phenylbutazone, diclofenac or indomethacin (10(-4)-10(-3) M) in the nutrient also significantly inhibited the effects of both stimulants. In contrast, p.o. pretreatment with SA (100 mg/kg b.i.d. for 3 days and 1 h before removal of the colon) did not affect stimulatory properties of FK and ACh. SA given with the nutrient exerted a substantial inhibition of the stimulated tone. One-hour washout was sufficient to completely abolish the inhibitory action of SA but reduced that of ASA by only 25%. The data suggest that endogenous prostaglandins and/or thromboxanes are involved in the FK- and ACh-stimulated contraction of rat colonic smooth muscles.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine↗
[Cimetidine versus antacids].
The rationale of ulcer therapy with cimetidine or antacids is to block or neutralize gastric acid secretion intragastrically. 5 tablets of cimetidine can inhibit gastric acid secretion in duodenal ulcer patients by more than 50% over a 24-hour period. Approximately 250 ml per day of a highly active antacid is necessary to achieve a similar effect. The effect of cimetidine on night secretion is superior. In acute ulcer attack cimetidine brings about healing of the ulcer in duodenal ulcer disease in about 80% of all patients in about 4-6 weeks, and a maintenance dose of 200 mg in the evening may prevent a recurrence within a year in about 50% of all patients. According to American studies, antacid therapy in the above-mentioned dosage may achieve a similar healing rate in duodenal ulcer patients in acute attack. However, it is unknown whether high antacid therapy prevents ulcer recurrences. If acceptability of the treatment by the patient, side effects and costs are taken into account, cimetidine appears to be superior to high doses of antacid. However, it must be considered that in many European countries, including Switzerland, the spontaneous healing rate is up to 60% in placebo studies. It is thus legitimate to continue treating uncomplicated ulcers with the small antacid doses customary in Europe.
Antacids↗
A double-blind trial of loperamide in the treatment of chronic diarrhoea.
A new antidiarrhoeal compound, loperamide (Imodium; (Janssen) Ethnor) has been evaluated in the treatment of patients with chronic nonspecific diarrhoea. In a double-blind trial its effect was compared with that of a placebo. The results of this trial indicate that loperamide is an effective antidiarrhoeal compound.
Adolescent↗
Effects of prolonged administration of metiamide on serum gastrin, gastrin content of the antrum and gastric corpus, and G-cell population in the rat.
The effect of prolonged metiamide administration on serum gastrin, gastrin content of the antrum and gastric corpus, and G-cell population was studied in the rat. A single subcutaneous injection of metiamide (200 mg/kg) at the onset of 16 days of continous treatment with three daily injections was followed by a fivefold increase in serum gastrin level at 4 hr in fasted and at 4 and 6 hr in fed rats. After 16 days of metiamide, the fed rats showed a peak in serum gastrin level of the same magnitude as on day 1, but only at 4 hr. Two hours later, the levels decreased rapidly to basal values. In the fasted animals, the response to metiamide was reduced to a threefold increase at 2 hr. There was no difference in gastrin content of the antrum and gastric corpus nor in volume density of the G-cells after the prolonged treatment compared with the controls. It is concluded that in spite of rises in serum gastrin, prolonged metiamide medication has no effect on the gastrin content of the antrum and gastric corpus nor on the G-cell population in the rat. Furthermore, after prolonged treatment, metiamide-induced gastrin release is diminished.
Animals↗
[Effect of duodenal acidification on plasma secretin and pancreatic polypeptide in man (author's transl)].
Plasma secretin and pancreatic polypeptide has been measured in 10 normal volunteers before and after intraduodenal acidification. Secretin rose rapidly from 1,4 +/- 0,44 to 11,2 +/- 1,24 pmol/l (+/- SEM). PP also rose significantly from 39,0 +/- 3,0 to 52.3 +/- 5,8 pmol (paired p less than 0.01) but much slower and to a lesser extent than seen after a meal. This supports the conclusion that acid plays no important role in control of postprandial PP release.
Adult↗
[6 years experience with endoscopic retrograde cholangiopancreatography].
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Cholangiography↗
[Endoscopic papillotomy, alternative or supplement? (Study on 60 cases)].
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Adolescent↗