omeprazole, Prilosec
Effect of cimetidine and omeprazole on gastric ulcer healing of rats with limited food intake time.

Ito M, Segami T, Tsukahara T, Kojima R, Suzuki Y.

Department of Pharmacology, Faculty of Pharmacy, Meijo University, Nagoya, Japan.

The effects of cimetidine, omeprazole and atropine sulfate on the healing of acetic acid-induced gastric ulcers in rats with limited food intake time (9:00-10:00 a.m. and 5:00-6:00 p.m.) were evaluated 15 days after the acid injection. Oral repeated administration of cimetidine (25-100 mg/kg twice daily) or omeprazole (10-50 mg/kg once daily) dose dependently accelerated ulcer healing. Atropine sulfate (10 mg/kg twice daily, p.o.) was ineffective. A single oral administration of omeprazole (50 mg/kg) or cimetidine (100 mg/kg) resulted in potent and long-lasting anti-acid secretory and gastrin-releasing actions. The degree and duration of anti-acid secretion by atropine sulfate were equal to those of cimetidine, but the elevation of gastrin release by atropine sulfate was weak and temporary. These results indicate that the gastric ulcers of rats with a limited food intake time are useful for evaluating the healing effects of cimetidine and omeprazole on gastric ulcers. In addition, the effects of both drugs may be related to the increased gastrin release rather than to the reduced acid secretion.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7843261&dopt=Abstract omeprozole Prilosec



omeprazole, Prilosec
Cimetidine and omeprazole accelerate gastric ulcer healing by an increase in gastrin secretion.

Ito M, Segami T, Inaguma K, Suzuki Y.

Department of Pharmacology, Faculty of Pharmacy, Meijo University, Nagoya, Japan.

Daily oral administration of cimetidine or omeprazole markedly accelerated the healing of acetic acid-induced gastric ulcers in rats with a limited food intake time. The increased gastric acid secretion induced by daily treatment with histamine affected neither the spontaneous healing of the ulcers nor the healing-promoting actions of both agents. Pretreatment of rats with ulcers with 6-hydroxydopamine significantly inhibited the increase in the antrum gastrin cells, serum gastrin levels and corpus mucosal thickness elicited by repeated administration of cimetidine or omeprazole. Pretreatment with 6-hydroxydopamine did not affect the inhibitory actions of cimetidine and omeprazole on acid secretion, but completely abolished the ulcer healing-promoting actions of both drugs. Daily intraperitoneal administration of pentagastrin accelerated ulcer healing. These results suggest that cimetidine and omeprazole mainly accelerate the healing of gastric ulcers by the trophic action of gastrin via the increase in gastrin secretion, while the inhibition of acid secretion may play a minor role in ulcer healing.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7843262&dopt=Abstract omeprozole Prilosec



omeprazole, Prilosec
Effect of repeated boluses of intravenous omeprazole and primed infusions of ranitidine on 24-hour intragastric pH in healthy human subjects.

Teyssen S, Chari ST, Scheid J, Singer MV.

Department of Medicine IV (Gastroenterology), University Hospital of Heidelberg at Mannheim, Germany.

The aim of this study was to identify dosage regimens using intravenous omeprazole and ranitidine that would elevate and consistently maintain intragastric pH > 6 in the first 24 hr of therapy. In 19 healthy, fasting human subjects using continuous 24-hr gastric pH-metry, we studied two dosages of primed infusions of ranitidine (50 mg bolus followed by infusion of either 3 or 6 mg/kg body wt/24 hr) and six regimens of intravenous omeprazole (80-200 mg in 24 hr in two to five boluses). Only the two ranitidine infusions and high doses of omeprazole (> or = 160 mg/day as four or five boluses) raised the intragastric median pH above 5.4. There was no significant difference in the median intragastric pH after high dose ranitidine and high doses of omeprazole. Considerable interindividual variation in intragastric pH was observed after omeprazole therapy. The percentage of intragastric pH > 6.0 during the 24-hr study was lower after omeprazole (35-42%) than after high-dose ranitidine (58%). We conclude that it is possible to raise intragastric pH > 6.0 by use of either primed ranitidine infusion or by repeated boluses of omeprazole. However, maintenance of this high pH in the first 24 hr is difficult with both, more so with omeprazole.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7851185&dopt=Abstract omeprozole Prilosec



omeprazole, Prilosec
Esomeprazole 40 mg i.v. provides faster and more effective intragastric acid control than pantoprazole 40 mg i.v.: results of a randomized study.

Wilder-Smith CH, Rohss K, Bondarov P, Hallerback B, Svedberg LE, Ahlbom H.

Gastroenterology Group Practice, GI Physiology Laboratory, Berne, Switzerland. cws ggp.ch

BACKGROUND: Oral esomeprazole 40 mg provides greater acid control than oral pantoprazole 40 mg. AIM: To compare the effects on intragastric acid control of esomeprazole 40 mg administered intravenously with pantoprazole 40 mg intravenously. METHODS: Healthy Helicobacter pylori-negative male and female subjects were enrolled into this single-centre, open, randomized, two-way crossover study. Esomeprazole 40 mg intravenously and pantoprazole 40 mg intravenously were administered as 15-min infusions once daily at 09:00 hours for 5 days. Continuous 24-h intragastric pH monitoring was carried out at baseline and on days 1 and 5. RESULTS: pH-data were available for all 25 subjects who completed the study. Esomeprazole 40 mg intravenously resulted in 8.3 and 13.9 h with an intragastric pH > 4 on days 1 and 5 compared with 5.3 and 9.0 h, respectively for pantoprazole 40 mg intravenously (day 1: P < 0.001, day 5: P < 0.0001). During the first 4 h of dosing on day 1 corresponding values were 1.7 and 0.6 h respectively (P < 0.0001). A mean median pH above 4 on day 5 was only attained with esomeprazole 40 mg intravenously. CONCLUSIONS: Once-daily dosing with esomeprazole 40 mg intravenously provides faster and more pronounced intragastric acid control than pantoprazole 40 mg intravenously.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15569112&dopt=Abstract omeprozole Prilosec



omeprazole, Prilosec
Omeprazole treatment of children with peptic esophagitis refractory to ranitidine therapy.

Karjoo M, Kane R.

Cardinal Glennon Children's Hospital, Saint Louis University School of Medicine, Mo.

OBJECTIVE: To evaluate the cause of chronic abdominal pain lasting more than 3 weeks in 153 patients aged 6 to 18 years (mean, 9.9 years) who had undergone endoscopy. DESIGN: Those patients with peptic esophagitis as the cause of their chronic pain were treated with high-dose ranitidine hydrochloride, followed by the proton-pump inhibitor, omeprazole, for those who did not respond to a histamine2-receptor antagonist. RESULTS: Eighty-four percent of patients had peptic esophagitis, 3% had Helicobacater pylori gastritis, and 3% had ulcer disease. Seventy percent of the patients with peptic esophagitis responded to an 8-week course of high-dose ranitidine hydrochloride (4 mg/kg per dose, twice a day or three times a day). Of the 30% of patients who failed to respond to ranitidine therapy, 87% responded to an 8-week course of omeprazole (20 mg/d). The grade of esophagitis at initial endoscopy was a predictive factor for response to ranitidine therapy. Ninety percent of patients with grade 1 esophagitis responded to ranitidine therapy vs only 43% of those with grade 3 or 4 esophagitis. Only five patients (4%) failed to respond to both therapies; three of these subsequently underwent Nissen fundoplications. There were no side effects of either ranitidine or omeprazole therapy. CONCLUSIONS: These findings indicate that (1) peptic esophagitis was a common cause of chronic abdominal pain in pediatric patients and (2) omeprazole was effective in the treatment of esophagitis in children and adolescents that was resistant to high-dose histamine2-receptor antagonists.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7858685&dopt=Abstract omeprozole Prilosec



omeprazole, Prilosec
Classification of dyspepsia and response to treatment with proton-pump inhibitors.

Meineche-Schmidt V.

General Practice, Klampenborg, Denmark. villy strandvang.dk

BACKGROUND: Lacking an objective 'gold standard' for diagnosing dyspepsia, several symptom-based classifications have been suggested. AIM: To assess if response to proton-pump inhibitor treatment could provide useful information for current or future dyspepsia classification. METHODS: Post hoc analyses of 829 patients treated with omeprazole or placebo in a randomized-controlled trial. The 'true' response to omeprazole (trial response minus placebo response) was assessed according to different classifications of dyspepsia and different symptoms. RESULTS: Symptoms described with the words 'burning' or 'sour' and patients with reflux-like dyspepsia demonstrated high response to omeprazole treatment, whereas patients with abdominal pain or ulcer-like dyspepsia responded unpredictably to omeprazole. The response to omeprazole in patients with epigastic pain was related to the pattern of other dyspeptic symptoms. Patients with heartburn or regurgitation overlapped extensively with patients with epigastric pain. CONCLUSION: The study demonstrated significant problems in the current classification of dyspepsia: 'the most bothersome symptom' was not independently related to the omeprazole effect and, in patients with abdominal pain, the response to omeprazole was dependent on the presence or absence of other dyspeptic symptoms. The overlap of symptoms indicates that heartburn and regurgitation should be recognized as symptoms of dyspepsia in primary care.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15569120&dopt=Abstract omeprozole Prilosec



omeprazole, Prilosec
Changes in the intragastric distribution of Helicobacter pylori during treatment with omeprazole.

Logan RP, Walker MM, Misiewicz JJ, Gummett PA, Karim QN, Baron JH.

Parkside Helicobacter Study Group, Central Middlesex Hospital, London.

Omeprazole is a powerful inhibitor of gastric acid and may suppress Helicobacter pylori by effecting the pKa of H pylori urease, by altering the pattern of infection, or by promoting overgrowth of other bacteria. At routine endoscopy H pylori was detected by histology and culture before and after four weeks' treatment with omeprazole, 40 mg each morning. A 13C-urea breath test was also done at t = 0, 2, 4, and 6 weeks. Thirty nine patients with duodenal ulcer (n = 25) or reflux oesophagitis (n = 14) were studied, of whom 29 of 39 had H pylori infection. During omeprazole treatment, 13C-urea breath test values fell significantly--mean (SEM) values before treatment and at four weeks were 23.0 (2.1) and 15.5 (2.7) per mil respectively, p < 0.001. Before treatment H pylori was seen in 28 of 29 antral, 29 of 29 corpus, and 28 of 29 fundic biopsy specimens. After four weeks of omeprazole treatment, the histological density of H pylori in the antrum and corpus was reduced (p < 0.001), while that in the fundus was increased. The migration of H pylori from the antrum to the fundus was associated with a corresponding decrease in the activity of antral gastritis. H pylori was not seen in antral biopsy specimens from 12 of 29 patients whose median excess delta 13CO2 excretion fell from 23.0 to 9.9 per mil. In the body mucosa, 26 of 29 specimens were still positive for H pylori and there was no significant change in the gastritis type. Two weeks after finishing treatment, the mean (SEM) excess delta 13CO2 excretion returned to levels before treatment. Omeprazole decreases antral H pylori colonisation but increases that in the fundus. The changes in the intragastric distribution of the organism are associated with concomitant changes in the activity of gastritis and are matched by a progressive fall in the excretion of delta 13CO2.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7890214&dopt=Abstract omeprozole Prilosec



omeprazole, Prilosec
Protective action of omeprazole against gastric mucosal injury induced by hemorrhagic shock in rats.

Blandizzi C, Gherardi G, Natale G, Marveggio C, Del Tacca M.

Institute of Medical Pharmacology, University of Pisa, Italy.

The efficacy of omeprazole in preventing gastric mucosal injury induced by hemorrhagic shock in rats and the putative mechanisms involved in this effect were investigated in the present study. Omeprazole did not affect mean arterial blood pressure under both basal conditions and induction of hemorrhagic shock, but it evoked a marked increase in Alcian blue recovery from gastric preepithelial mucus. The morphometric analysis of histological sections revealed that omeprazole caused a significant reduction of hemorrhagic shock-induced damage of gastric mucosa. Ranitidine, used as the reference drug, failed to affect mean arterial blood pressure, Alcian blue recovery from gastric mucus, or hemorrhagic shock-induced damage of gastric mucosa. Both omeprazole and ranitidine exerted a significant inhibition of gastric acid output from anesthetized pylorus-ligated rats. Overall, the present results indicate that omeprazole is effective in protecting gastric mucosa from necrotic damage induced by hemorrhagic shock and suggest that an enhancement of gastric mucus secretion contributes to this protective action.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7924729&dopt=Abstract omeprozole Prilosec