Drugs online research references
Pharmacol Res. 1994 Jan-Feb;29(1):47-58.
Effects of omeprazole on ethanol metabolism: an in vitro and in vivo rat and human study.
Pozzato G, Franzin F, Moretti M, Lachin T, Benedetti G, Sablich R, Marin M, Stebel M, Campanacci L.
Institute of Patologia Medica, University School of Medicine, Trieste, Italy.
Since some H2-receptor antagonists, like cimetidine or ranitidine, affect ethanol metabolism by interference with gastric and/or hepatic alcohol dehydrogenase (ADH) it was investigated whether omeprazole has a similar effect and its effects were compared with those of cimetidine, an inhibitor of gastric ADH. The first-pass metabolism (FPM), quantified by measuring the difference between areas under the curve (AUC) of ethanol blood concentrations after oral intake or intravenous administration of the same amount (0.3 g kg-1 b.w.) of ethanol (EtOH), was studied before and after 1 week of omeprazole (20 mg daily) or cimetidine (800 mg daily) administration in 10 normal male volunteers. ADH activity was determined in gastric mucosal samples, collected during endoscopy, before and after 1 month of omeprazole treatment. The effect of the drugs on gastric and hepatic ADHs was studied in vitro in both rat and man. No significant effect of omeprazole was found on AUCs of the blood EtOH concentrations. The ADH activity in antral mucosa before and after omeprazole therapy did not show significant differences. In vitro, omeprazole reduced the activity of the low Km gastric ADH with a Ki of 5.6 mM in rat and the hepatic ADH activity with a Ki of 2.4 mM in man, whereas the drug did not show any effect on hepatic ADH in rat and gastric ADH in man. On the contrary, cimetidine increased the AUCs of EtOH blood concentrations after both gastric and intravenous route and, in the in vitro assay, inhibited gastric and hepatic ADH in both man and rat. These results indicate that omeprazole does not affect EtOH metabolism in man and seems to be safer than cimetidine in subjects unable to reduce ethanol intake during the therapy for peptic ulcer or other hypersecretory conditions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8202442&dopt=Abstract
note: kwd match prilosec online literature
Pharmacol Res. 1995 May;31(5):305-11.
Hepatic glutathione after ethanol administration in rat: effects of cimetidine and omeprazole.
Battiston L, Tulissi P, Moretti M, Mazzoran L, Marchi P, Pussini E, Pozzato G.
Institute of Medicina Clinica, University of Trieste, School of Medicine, Italy.
As a fraction of ingested ethanol (EtOH) is metabolized by gastric mucosa, different amounts of alcohol reach the liver, when the same dose is administered by oral or intravenous route. In previous experiments, we demonstrated that the decrease of hepatic reduced glutathione (GSH) is less pronounced and is followed by a quicker recovery after oral than after intraperitoneal administration of the same amount of EtOH. Therefore, the time-course of hepatic GSH concentration seems to be an indirect assay of EtOH metabolism by the liver. On the basis of these findings, any condition causing a reduced function of gastric alcohol dehydrogenase (ADH) should show up as a more severe depletion of hepatic GSH. In the same rat experimental model we determined the effects of cimetidine and omeprazole administration on gastric ADH activity and on the time-course of hepatic GSH after EtOH load. Cimetidine was shown to inhibit gastric ADH with a Ki of 0.167 +/- 0.009 mmol l-1; accordingly, the pretreatment with this drug (20 mg kg-1 b.w. per day for 1 week) determined, after oral EtOH load, a marked reduction of hepatic GSH, likewise after intraperitoneal administration. Omeprazole exerted only a marginal inhibition on gastric ADH and this drug (0.3 mg kg-1 b.w. per day for 1 week) did not modify the time-course of hepatic GSH concentrations after EtOH load. This study indicates that the inhibition of gastric ADH, when associated with EtOH intake, induces depletion of the hepatic GSH concentration and, therefore, possible liver damage.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7479528&dopt=Abstract
note: kwd match prilosec online literature
J Clin Gastroenterol. 1995;20 Suppl 2:S5-7.
Effects of lansoprazole on ethanol-induced injury and PG synthetic activity in rat gastric mucosa.
Fukuda T, Arakawa T, Shimizu Y, Ohtani K, Higuchi K, Kobayashi K.
Third Department of Internal Medicine, Osaka City University Medical School, Japan.
Lansoprazole, a proton pump inhibitor, has been reported to inhibit ethanol-induced injury in rats. However, the mechanism of the protective effect is not known. This study was carried out to investigate the role of prostaglandin (PG) in the protective effect of lansoprazole. Male Wistar rats were given either 30 mg/kg of lansoprazole or vehicle alone intragastrically 30 min before administration of ethanol. They were killed to measure the gross mucosal lesions in the stomach as the ulcer index. In another experiment, 5 mg/kg of indomethacin was injected 30 min before administration of lansoprazole. The effects of 16,16-dimethyl PGE2 (dmPGE2) on ethanol-induced injury over time were compared with lansoprazole. PGE2 synthesis in gastric mucosa after administration of lansoprazole was measured by radioimmunoassay. Lansoprazole reduced gastric mucosal injury by lansoprazole. DmPGE2 significantly reduced gastric mucosal injury from 5 min after exposure to ethanol. Lansoprazole did not affect PGE2 synthesis in the gastric mucosa. These results suggest that PG may not be involved in the protective effect of lansoprazole.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7594340&dopt=Abstract
note: kwd match prilosec online literature
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