Drugs online research references
Aliment Pharmacol Ther. 1991 Aug;5(4):405-12.
Effect of omeprazole on intestinal output in the short bowel syndrome.
Nightingale JM, Walker ER, Farthing MJ, Lennard-Jones JE.
St Mark's Hospital, London, UK.
Ten patients with an end jejunostomy and one with a jejuno-rectal anastomosis (jejunal length 30-140 cm) ate a constant chosen diet for 2 control days, and 2 test days when 40 mg omeprazole orally was taken each morning. In the 7 patients with a net secretory output of fluid, there was a mean reduction in wet weight of 0.66 kg/24 h (range -0.16 to 1.45 kg/24 h; P less than 0.05) and sodium 46 mmol/24 h (-51 to 135 mmol/24 h; N.S.); the four patients with net absorption of fluid showed no reduction in intestinal output. One patient with 30 cm jejunum responded little to oral but did so to intravenous 40 mg omeprazole twice a day with a reduction in wet weight of 3.00 kg/24 h and sodium 157 mmol/24 h. In one patient oral 40 mg omeprazole daily gave equivalent results to oral 300 mg ranitidine twice daily; in 2 others it was equivalent to intravenous 50 micrograms octreotide twice daily. Omeprazole reduces the intestinal output in patients with the short bowel syndrome and a net secretory output, but not enough to prevent the need for parenteral fluid and electrolyte replacement.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1777549&dopt=Abstract
note: kwd match prilosec online literature
Nippon Rinsho. 1992 Jan;50(1):18-25.
[Studies on the intracellular pharmacodynamic properties of proton pump inhibitors and the inhibitory mechanism of acid secretion]
[Article in Japanese]
Saito E, Matsuo Y.
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo.
In recent studies, proton pump inhibitors, such as omeprazole, were found to be transformed into sulfenamide derivatives in the acid space of isolated parietal cells. It is considered that these sulfenamide derivatives mainly inhibit H+, K(+)-ATPase activity. To clarify the inhibitory mechanism of proton pump inhibitors, we studied the effect on acid secretion of the isolated parietal cells. Proton pump inhibitors inhibited histamine-, carbachol- and gastrin-stimulated 14C-aminopyrine accumulation. Db-cAMP stimulation was also inhibited by these inhibitors. Consequently, it is believed that the origin of H+, K(+)-ATPase was located in the final stage of the acid production.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1311783&dopt=Abstract
note: kwd match prilosec online literature
Scand J Gastroenterol Suppl. 1985;108:95-104.
Localization of omeprazole and metabolites in the mouse.
Helander HF, Ramsay CH, Regardh CG.
Omeprazole is a substituted benzimidazole which blocks gastric acid secretion by inhibiting H+K+ATPase. Radioactive omeprazole was given intravenously or orally to mice, and the distribution of the drug was investigated at various intervals by scintillation counting and by autoradiography. The half-life for radioactivity in the stomach was 14 hours versus 30-36 hours in the liver, kidneys and blood. At 16 hours after the drug was given, the radioactivity in the stomach was ten times higher than that in the liver and kidneys, and 100 times that in the blood. Whole-body autoradiography showed sustained high levels of radioactivity only in the gastric mucosa. Light microscopic autoradiographic investigations of the gastric mucosa from mice killed 1 or 16 hours after the drug was given revealed radioactivity in the parietal cells. By electron microscopy of gastric mucosa from the mouse killed 16 hours after omeprazole injection the isotope label was found mainly over the secretory surface and the tubulo-vesicles. At these locations H+K+ATPase has previously been demonstrated, and it is suggested that omeprazole--or its metabolites--binds to this enzyme.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3858979&dopt=Abstract
note: kwd match prilosec online literature
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