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  • 1
    Electronic Resource
    Electronic Resource
    Gastric and cardiovascular effects of histamine in the dog (1979)
    Springer
    Inflammation research 9 (1979), S. 428-434 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The H-2 receptor stimulation of gastric acid secretion and of heart rate by histamine, a mixed H-1–H-2 agonist, given in 45-min successive step doses 2–150 μg base/kg.h and 4(Me)histamine, (4(Me)H), 1.4 to 210 μg base/kg.h, a specific H-2 agonist, in five conscious gastric fistula dogs showed no difference between the agonists in ED50s or in maximal responses. The ED50 for acid was lower (15–16 μg/kg.h) than for cardiac chronotropism (25 to 27 μg/kg.h). Both effects were competitively antagonized by the H-2 antagonist cimetidine, 0.5 to 1 mg/kg.h. Background infusions of diphenhydramine, 2 mg/kg.h, raised the maximum heart rate increase caused by histamine from +108 to +149 beats/min (p〈0.05) but not that of 4(Me)H; acid outputs were not augmented. Diphenhydramine 2 mg/kg.h alone caused no significant change in heart rate or blood pressure. Histamine reduced systolic blood pressure (SBP) by 48 mmHg and with diphenhydramine background by 61 mmHg (p〈0.05). 4(Me)H at a top dose of 210 μg base/kg.h reduced SBP by 81 mmHg (p〈0.05). To test whether the effects of added diphenhydramine could be interpreted as an H-1 receptor effect of histamine, the H-1 agonist 2-pyridylethylamine (PEA) was given alone (2–150 μg/kg.h in 45-min steps) or as a 100 μg/kg bolus during the infusion of 4(Me)H 50 μg/kg.h. There was no effect of PEA on gastric acid, heart rate or blood pressure. Even though diphenhydramine augments the effect of histamine on heart rate and blood pressure, the lack of PEA effect would indicate that there is not a direct H-1 receptor mediated effect on gastric acid, heart rate or systolic blood pressure in the conscious dog. This contrasts with published data obtained in anesthetized animals. After a single dose of 4(Me)H, 50 μg/kg.h had been infused i.v. for 45 min, acid output had reached 70% of the maximum seen at 90 min, heart rate had increased by 65% of its maximum response but SBP had not yet changed. Cimetidine blocked 4(Me)H-induced hypotension completely but blocked the heart rate increase only partially and competitively. We conclude that in the intact animal there is evidence for a direct H-2 mediated stimulation of heart rate in the conscious dog with kinetics similar to the H-2 stimulation of gastric acid secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01968106
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  • 2
    Electronic Resource
    Electronic Resource
    H-2 Histamine Receptors (1979)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Pharmacology 19 (1979), S. 203-244 
    Details
    ISSN: 0362-1642
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.pa.19.040179.001223
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  • 3
    Electronic Resource
    Electronic Resource
    Long-term treatment with lansoprazole for patients with Zollinger–Ellison syndrome (1996)
    Oxford BSL : Blackwell Science
    Alimentary pharmacology & therapeutics 10 (1996), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Normalization of gastric secretion and cure of associated upper gastrointestinal lesions by resection of gastrinoma is possible in ≈20% of patients with Zollinger–Ellison syndrome, leaving ≈80% dependent on medical treatment with proton pump inhibitors for acid suppression. Methods: Lansoprazole was given for 3–48 months (median 28 months) to 26 Zollinger–Ellison syndrome patients with peptic ulcer manifestations in all and oesophagitis in 13. Starting with 60 mg/day, the dose was individualized to lower basal acid output to less than 5 mmol/h for those with intact stomachs and less than 1 mmol/h in those who had prior gastrectomy or with oesophagitis. The patients were studied every 3 months for 1 year and then every 6 months with gastric analysis (basal and maximal acid and pepsin output) and endoscopy with biopsy for enterochromaffin-like (ECL) cells. Results: Lansoprazole inhibited basal acid output by 95%, pepsin output by 65% and remained effective at the initial mean (66±4.3 mg/day) or smaller doses (56±12 mg/day) at 48 months. Mucosal lesions healed and symptoms (ulcer-type pain, diarrhoea, heartburn, weight loss) resolved rapidly, usually within a few weeks. Serum gastrin and ECL cell populations, which were elevated before treatment, remained statistically unchanged but one of the three multiple endocrine neoplasia I (MEN-I) patients developed a small carcinoid. Of the three patients with metastatic gastrinoma at diagnosis one has died and one has progressed, while the third has had stable liver metastases for 26 years. Ulcer-type relapses occurred in three of the five post-gastrectomy patients, one with fatal jejunal ulcer perforation despite adequate acid suppression. No biochemical or clinical adverse events due to lansoprazole were encountered. Conclusion: Lansoprazole effectively inhibits acid and pepsin secretion in Zollinger–Ellison syndrome patients without any demonstrated side-effects. Despite strict acid control, post-gastrectomy Zollinger–Ellison syndrome patients were more liable to ulcer relapse, while oesophagitis was not a marker for therapeutic difficulty.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.1996.10152000.x
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  • 4
    Electronic Resource
    Electronic Resource
    Long-term lansoprazole control of gastric acid and pepsin secretion in ZE and non-ZE hypersecretors: a prospective 10-year study (2001)
    Oxford UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 15 (2001), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The majority of patients with Zollinger–Ellison syndrome require lifelong treatment with proton pump inhibitors.〈section xml:id="abs1-2"〉〈title type="main"〉Aims:To determine the efficacy of lansoprazole control of acid and pepsin secretion over the long term in Zollinger–Ellison syndrome and non-Zollinger–Ellison syndrome hypersecretors.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Sixty-three hypersecretors (basal acid output 〉 15 mmol/h), 46 Zollinger–Ellison syndrome and 17 non-Zollinger–Ellison syndrome, with a total history of 15.4 and 19.2 years, respectively, were entered into a long-term prospective study using lansoprazole. Sixty-one were studied every 3 months for 1 year and then every 3–6 months up to 10 years during lansoprazole treatment with endoscopy, serum gastrin and gastric analysis, measuring both basal and stimulated pH and acid and pepsin secretion. Doses were individually optimized and adjusted to keep the basal acid output at 〈 5 mmol/h in intact patients and 〈 1 mmol/h in antrectomized Zollinger–Ellison syndrome patients.〈section xml:id="abs1-4"〉〈title type="main"〉Results:The dose of lansoprazole could not be predicted a priori from pre-treatment acid or pepsin output, serum gastrin, prior omeprazole dose or diagnosis or prior complications. The median dose was ∼ 80 mg/day, with a wide range from 15 mg every other day to 360 mg/day, and generally stabilized by 12 months. However, as doses were adjusted over time for indications, almost half the patients required higher doses. With adjustments, the basal acid output was maintained in the target range in 〉 90% of intact patients and in 80% of antrectomized patients. Gastric juice pH increased from ∼ 1.2 before therapy to 〉 3.4 during therapy. Serum gastrin in Zollinger–Ellison syndrome patients, after excluding five outliers, did not change over the course of therapy, but doubled in non-Zollinger–Ellison syndrome patients. There were no adverse events due to lansoprazole, and routine laboratory studies remained normal.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions:The dose of lansoprazole for hypersecretors cannot be predicted, and thus needs to be optimized empirically on an individual basis. With continued periodic adjustments, almost half the patients required increased doses, while safe dose reduction was possible in only one-quarter. When individually optimized, lansoprazole proved to be safe and effective in the control of secretion for the treatment of both Zollinger–Ellison syndrome and non-Zollinger–Ellison syndrome hypersecretors for up to 10 years.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2001.01097.x
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  • 5
    Electronic Resource
    Electronic Resource
    Minor effects of Helicobacter pylori on gastric secretion and dose of lansoprazole during long-term treatment in ZE and non-ZE acid hypersecretors (2002)
    Oxford UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 16 (2002), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Helicobacter pylori infection may increase or decrease acid secretion and may augment proton pump inhibitor efficacy. Pepsin effects have not been reported. In Zollinger–Ellison syndrome (ZE) specifically, H. pylori has been reported to decrease acid.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To examine H. pylori effects on secretion and dose of medication in hypersecretors (basal acid output 〉 15 mmol/h) undergoing long-term treatment with individually optimized lansoprazole doses.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Sixty-five patients (47 ZE and 18 non-ZE), treated for 〉 3 months to 10 years, were tested every 6 months with endoscopy, gastric analysis and serum gastrin.〈section xml:id="abs1-4"〉〈title type="main"〉Results:Forty-three per cent were H. pylori-positive. Acid, pepsin and gastrin were not different between H. pylori-positive and H. pylori-negative patients before or during long-term lansoprazole treatment. Initially, H. pylori-positive patients required less lansoprazole than H. pylori-negative patients (68 ± 6 vs. 96 ± 8 mg/day), but after 3 years the doses converged (83 vs. 86 mg/day). The disappearance of H. pylori in 15 patients caused no significant changes in acid, pepsin, gastrin or lansoprazole dose in the following 4 years.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions: H. pylori had no significant initial or long-term physiological or potential clinical effects on acid or pepsin secretion or gastrin in these acid hypersecretors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2002.01175.x
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  • 6
    Electronic Resource
    Electronic Resource
    Helicobacter pylori effects on gastritis, gastrin and enterochromaffin-like cells in Zollinger–Ellison syndrome and non-Zollinger–Ellison syndrome acid hypersecretors treated long-term with lansoprazole (2001)
    Oxford UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 15 (2001), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Helicobacter pylori is said to cause atrophy of the gastric corpus and enterochromaffin-like cell proliferation in gastro-oesophageal reflux disease (GERD) patients treated long-term with a proton pump inhibitor.〈section xml:id="abs1-2"〉〈title type="main"〉Aims:To determine the effect of H. pylori infection on gastritis, enterochromaffin-like cell density and hyperplasia, mucosal atrophy and serum gastrin in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h) with either hypergastrinemia (Zollinger–Ellison syndrome) or normal gastrin (non-Zollinger–Ellison syndrome) before and during long-term treatment with lansoprazole.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Lansoprazole was individually titrated to reduce basal acid output to 〈 5 mmol/h (〈 1 mmol/h in post-surgical Zollinger–Ellison syndrome). Gastric corpus biopsies were obtained every 6 months before treatment and up to 8 years later.〈section xml:id="abs1-4"〉〈title type="main"〉Results: H. pylori was present in corpus biopsies in ≈ 50%, causing active gastritis which resolved rapidly in 15 subjects after elimination of H. pylori. Patchy mild/moderate corpus atrophy was present at entry in two and at the end in four out of 60 patients, one being H. pylori-positive. Intestinal metaplasia (〈 10%) was seen in six isolated biopsies (1% of total). H. pylori did not affect serum gastrin, enterochromaffin-like cell density or hyperplasia. Enterochromaffin-like cell density was twice as high in Zollinger–Ellison syndrome as in non-Zollinger–Ellison syndrome patients (241 vs. 126 cells/mm2, P 〈 0.001). Enterochromaffin-like cells remained normal in the non-Zollinger–Ellison syndrome hypersecretors regardless of H. pylori status.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion:Corpus enterochromaffin-like cell increases were related to serum gastrin elevation, but neither H. pylori nor long-term treatment with lansoprazole alone or together had any effect on enterochromaffin-like cell density or hyperplasia. Corpus acute gastritis resulted from H. pylori infection, but did not result in mucosal atrophy despite long-term proton pump inhibitor treatment and promptly resolved with loss of H. pylori.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2001.00876.x
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  • 7
    Electronic Resource
    Electronic Resource
    Daily omeprazole surpasses intermittent dosing in preventing relapse of oesophagitis: a US multi-centre double-blind study (1997)
    Oxford BSL : Blackwell Science
    Alimentary pharmacology & therapeutics 11 (1997), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Introduction: Relapse of erosive oesophagitis occurs in almost all patients if treatment is stopped after initial healing. Aim: To assess the potential of different therapeutic regimens of omeprazole to prevent relapse of erosive reflux oesophagitis after initial healing with omeprazole. Patients and methods: Patients whose active erosive reflux oesophagitis (grade 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:02692813:APT141:ges" location="ges.gif"/〉2) had healed (grade 0 or 1) after 4–8 weeks of open-label omeprazole 40 mg daily (phase I) were eligible to join a multi-centre, 6-month double-blind, placebo-controlled maintenance study (phase II), which included endoscopy, symptom assessments, serum gastrin measurements, and gastric fundic biopsies. During phase I, endoscopy was performed at weeks 0, 4, and 8. At the end of phase I, 429 of 472 patients (91%) were healed, and there were significant reductions in heartburn, dysphagia and acid regurgitation. Of the 429 patients who healed, 406 joined phase II and were randomized to one of three groups: 20 mg omeprazole daily (n=138), 20 mg omeprazole for 3 consecutive days each week (n=137), or placebo (n=131). During phase II, endoscopy was performed at months 1, 3, and 6 or at symptomatic relapse. Results: The percentages of patients still in endoscopic remission at 6 months were 11% for placebo, 34% for omeprazole 3-days-a-week, and 70% for omeprazole daily. Both omeprazole regimens were superior to placebo in preventing recurrence of symptoms (P〈0.001); however, omeprazole 20 mg daily was superior to omeprazole 20 mg 3-days-a-week (P〈0.001). Compared to baseline, omeprazole therapy resulted in no significant differences among treatment groups in the distribution of gastric endocrine cells. Conclusions: These results show that after healing of erosive oesophagitis with 4–8 weeks of omeprazole, relapse of oesophagitis and recurrence of reflux symptoms can be prevented in 70% of patients with a maintenance regimen of 20 mg daily, but that intermittent dosing comprising 3 consecutive days each week significantly compromises efficacy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.1997.141317000.x
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  • 8
    Electronic Resource
    Electronic Resource
    Long-term treatment with lansoprazole of patients with duodenal ulcer and basal acid output of more than 15mmol/h (1996)
    Oxford BSL : Blackwell Science
    Alimentary pharmacology & therapeutics 10 (1996), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: About 10% of patients with duodenal ulcers have marked gastric acid hypersecretion with basal acid output (BAO) of more than 15 mmol/h, which is in the range found in Zollinger–Ellison syndrome. Patients and study design: We report long-term, up to 4 years, prospective treatment using lansoprazole in nine male patients with duodenal ulcers and a BAO of more than 15 mmol/h whose results are compared with those in 10 male Zollinger–Ellison syndrome patients with intact stomachs reported in detail in an accompanying paper. Results: All 19 subjects, except one Zollinger–Ellison syndrome patient who had gastric and oesophageal ulcers, had a history of duodenal ulcers; 22% of those with gastric acid hypersecretion had oesophagitis compared with 60% of those with Zollinger–Ellison syndrome. Each subject had the dose of lansoprazole adjusted to give a BAO of less than 5 mmol/h. At 3-month intervals to 1 year, and then at 6-monthly intervals, basal and pentagastrin stimulated secretions were studied, in addition to gastroscopy with biopsy for gastric mucosal morphology. Basal and maximal acid and pepsin secretions were not different between gastric acid hypersecretion and Zollinger–Ellison syndrome patients before treatment. During treatment, BAO was reduced by over 90% to less than 2 mmol/h, while peak acid output was reduced by 70% in those with gastric acid hypersecretion and 90% in Zollinger–Ellison syndrome patients. Four gastric acid hypersecretion patients had relapses during treatment, three times in one patient and twice in another patient, but all responded to continued treatment with lansoprazole. Of the seven ulcer-related relapses in the gastric acid hypersecretion patients, four occurred with a BAO of less than 2 mmol/h and three with a BAO of 7.1–7.3 mmol/h; five of the seven relapses occurred in the absence of Helicobacter pylori. Lansoprazole remained effective at an average dose of ≈70 mg/day, without causing any side-effects. Conclusion: Lansoprazole is apparently safe and effective for treating hypersecretion, whether due to hypergastrinaemia (Zollinger–Ellison syndrome) or not (non-Zollinger–Ellison syndrome hypersecretors).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.1996.11153000.x
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  • 9
    Electronic Resource
    Electronic Resource
    Effect of Therapeutic Doses of Colchicine on Oxidative Enzymes in the Intestine (1964)
    [s.l.] : Nature Publishing Group
    Nature 202 (1964), S. 608-609 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] We have shown in this laboratory that xylose absorption is significantly reduced after the administration of colchicine to the dog6 at a much lower dose (0-1-0-24 mg/kg). Thus we felt that a combined histochemical and biochemical study of colchicine action on the small intestine of mouse would be ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/202608a0
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  • 10
    Electronic Resource
    Electronic Resource
    Gastrin release in fistula dogs with solid compared to nutrient and nonnutrient liquid meals (1983)
    Springer
    Digestive diseases and sciences 28 (1983), S. 705-711 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using conscious gastric fistula dogs, gastrin release stimulated by a 360-g meat-based solid meal was compared to that stimulated by two isocaloric (1 kcal/g), hypertonic (∼700 mosm/kg) nutrient liquids (Sustacal and Vivonex) and by two nonnutrient, hypotonic (60 mosm/kg) liquids (mannitol and coffee). Serum gastrin levels were measured at 15- to 30-min intervals over 120 min. Without a meal, serum gastrin levels remained stable. Effectiveness in stimulating gastrin release was coffee = mannitol 〈 Sustacal = Vivonex 〈 solid food; 2-hr integrated gastrin responses were 1.2, 2.6, 4.3, 5.6, and 12.2 ng/ml/min, respectively. The greater gastrin responses produced by nutrient liquids and meat meals could be explained by slower emptying and delayed acidification of gastric contents. We conclude that solid meals are preferable to liquid meals in studies of antral gastrin release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01312560
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