Drugs online research references
Gastroenterology. 1993 Jun;104(6):1686-91.
Restoration of squamous mucosa after ablation of Barrett's esophageal epithelium.
Berenson MM, Johnson TD, Markowitz NR, Buchi KN, Samowitz WS.
Department of Internal Medicine, Salt Lake City Veterans Administration Medical Center, Utah.
BACKGROUND: Antireflux therapy has generally failed to induce regression of Barrett's epithelium. It was hypothesized that squamous epithelium could be restored if the columnar tissue was ablated while gastric acid secretion was suppressed. METHODS: Ten white men with Barrett's esophagus received 40 mg of omeprazole daily. Thereafter, every 2-5 weeks they underwent videotaped endoscopies to argon laser photoablate columnar tissue, obtain biopsy specimens, and assess results. Squamous re-epithelialization was assessed by correlation of videotapes and directed biopsies. RESULTS: Patients had one to eight areas ablated, totaling 0.5-12.0 cm2. Videotape assessments were corroborated by biopsy in all but one instance. Thirty-eight of 40 treatment locations partially or completely re-epithelialized with squamous tissue. Squamous regrowth appeared to occur by spread from contiguous squamous borders and de novo from glandular tissue. Regrowth was influenced by the extent of squamous borders and completeness of ablations. Nonablated glandular tissue persisted beneath squamous epithelium. CONCLUSIONS: Ablation of Barrett's epithelium and suppression of acid secretion facilitated squamous re-epithelialization. A progenitor cell within the metaplastic tissue has the potential to differentiate normally.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8500727&dopt=Abstract
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Aliment Pharmacol Ther. 1992 Jun;6(3):335-49.
Effects on the rat oxyntic mucosa of the histamine2-antagonist loxtidine and the H+, K(+)-ATPase inhibitor omeprazole.
Brenna E, Waldum HL, Sandvik AK, Schulze Sognen B, Kristensen A.
Institute of Cancer Research, Trondheim University Hospital, Norway.
The present study examined whether histamine could affect the growth of the enterochromaffin-like (ECL) cell and the parietal cell. The effects of the unsurmountable histamine H2-receptor antagonist loxtidine (80 mg/kg) and the H+, K(+)-ATPase inhibitor omeprazole (100 mumol/kg) were compared in female Sprague-Dawley rats. Both drugs were given by gavage once daily for 3 months. Omeprazole induced a more pronounced and sustained hypergastrinaemia than loxtidine. In spite of marked hypergastrinaemia during most of the day, even in the loxtidine-treated rats, the weights of the stomach and oxyntic mucosa were elevated only in the omeprazole-treated rats. The ECL cell density was slightly higher in the loxtidine- than in the omeprazole-treated rats. Both treatments elevated the gastrin-stimulated histamine release from the vascularly perfused stomach. The parietal cell density was unaffected by omeprazole treatment, whereas it tended to be reduced in the loxtidine-treated rats. Simultaneous administration of loxtidine and omeprazole reduced the sustained hypergastrinaemia induced by omeprazole given alone. The present study may indicate that histamine inhibits the growth of the ECL cell, but further studies are needed to elucidate if histamine has any trophic effect on the parietal cells.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1600050&dopt=Abstract
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Digestion. 1990;47 Suppl 1:35-8.
Omeprazole and the gastric mucosa.
Sachs G, Scott D, Reuben M.
Department of Physiology, UCLA.
The potential for either omeprazole or its sulphenamide to interact with DNA was investigated by incubating tritiated omeprazole at either neutral or acidic pH with either purified prokaryotic (Escherichia coli) or purified eukaryotic (salmon sperm) DNA. Each incubation was carried out for 30 min. The DNA was separated on agarose gels, stained with ethidium bromide, and the radioactivity in the DNA determined. No radioactivity was associated with the DNA on the gel with either prokaryotic or eukaryotic DNA or with either protocol. No interaction with the DNA was found, thus excluding the possibilities of base modification, DNA strand breakage or intercalation. It was concluded that neither omeprazole nor its gastric metabolites are genotoxic.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2093013&dopt=Abstract
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