Drugs online research references
J Steroid Biochem Mol Biol. 1995 Jun;52(6):567-73.
Luteolytic action of RU486: modulation of luteal 3 beta-hydroxysteroid dehydrogenase and 20 alpha-hydroxysteroid dehydrogenase activities in late pregnant rats.
Telleria CM, Stocco CO, Deis RP.
Laboratorio de Reproduccion y Lactancia, CRICYT-CONICET, Mendoza, Argentina.
The effect of the synthetic antiprogestin RU486 on luteal function in late pregnant rats was studied by evaluating the activities of the enzymes 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) and 20 alpha-hydroxysteroid dehydrogenase (20 alpha-HSD). RU486 (2 mg/kg) administered to rats on day 18 of pregnancy at 10.00 h induced preterm delivery 26.4 +/- 0.35 h (n = 8) after treatment. Luteal 3 beta-HSD activity increased 24 and 34 h after RU486 injection, but a significant and progressive decrease started at 48 h with the maximal reduction 72 h after RU486 treatment, when compared with controls. Serum progesterone concentration decreased at the time of 3 beta-HSD activity reduction. Interestingly, 20 alpha-HSD activity started to increase 58 h after RU486 injection. The administration of the cyclooxygenase inhibitor, diclofenac (1.3 mg/kg), on days 17-19 of pregnancy to RU486-treated rats, delayed abortion and the duration of delivery, and prevented the decrease in 3 beta-HSD and the increase in 20 alpha-HSD activities observed 58 h after antiprogesterone treatment. RU486 administered intrabursally (1 microgram per ovary) on day 20 (14.00-15.00 h) increased 3 beta-HSD and decreased 20 alpha-HSD luteal activities at 18.00 h on day 21 of pregnancy, without modifying serum progesterone concentration, when compared with normal pregnant rats. In conclusion, the luteolytic process after preterm delivery induced by RU486 administration in late pregnant rats is characterized by a decrease in luteal 3 beta-HSD activity and circulating progesterone, which may trigger the increase in luteal 20 alpha-HSD activity. Prostaglandins seems to be involved in the increase of 20 alpha-HSD activity and therefore, in the demise of corpora lutea.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7779760&dopt=Abstract
Acta Physiol Hung. 1992;80(1-4):281-7.
Measurement of non-steroid antiinflammatory drugs induced gastric microbleeding.
Bero T, Nagy L, Javor T, Vincze A.
First Department of Medicine, University Medical School, Pecs, Hungary.
The damage of the mucous membranes in the gastrointestinal tract caused by non-steroid antiinflammatory drugs are well known. The gastrointestinal microbleeding was measured by the method of Fischer and Hunt before and after the intake of indomethacin (4 x 25 mg), naproxen-sodium (4 x 275 mg), diclofenac (3 x 50 mg) and azapropazone (2 x 600 mg). In the indomethacin group microbleeding increased from 0.91 +/- 0.12 ml/24 h to 7.30 +/- 1.20 ml/h. In the naproxen-sodium group from 1.22 +/- 0.16 ml/24 h to 3.56 +/- 0.40 ml/24 h, in the diclofenac group from 0.86 +/- 0.14 ml/24 h to 3.18 +/- 0.28 ml/24 h, in azapropazone group from 0.92 +/- 0.18 ml/24 h to 2.50 +/- 0.20 ml/24 h, respectively. All non-steroid antiinflammatory drugs increased the gastric microbleeding, however, there were considerable differences in the degree of enhancement. This can be explained by the different inhibitory activities of the drugs on the cyclooxygenase enzyme activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1345197&dopt=Abstract
Dig Dis Sci. 1982 Jul;27(7):624-35.
Relationship of gastric mucosal damage induced in pigs by antiinflammatory drugs to their effects on prostaglandin production.
Rainsford KD, Willis C.
Experiments were performed in pigs to examine the relationship between the effects of various nonsteroid antiinflammatory drugs on gastric (fundic) mucosal content of prostaglandin (PG)E2 and 6-keto-PGF1 alpha, and the development of damage to the fundic mucosa under acute and chronic dosage conditions. Oral administration of a single dose of indomethacin (5 mg/kg) caused an almost immediate reduction in mucosal potential difference, followed at 5-15 min by ultrastructurally observed damage to mucosal capillaries, mucous, and parietal cells; efflux of Na+, K+, and Cl- ions into the gastric lumen with an apparent loss of luminal H+ ions; and a statistically significant reduction (from 10-60 min) in fundic prostaglandin content. Thus, under acute dosage conditions, development of mucosal damage by indomethacin was paralleled by the reduction in prostaglandin production. Repeated oral dosage of aspirin, indomethacin, sulindac, or diclofenac to pigs for 10 days significantly reduced gastric mucosal as well as plasma prostaglandin levels, coincident with the development of severe gastric mucosal damage. The relatively less irritant drugs, flufenamic acid, azapropazone, and fenclofenac, failed to significantly decrease gastric mucosal content of prostaglandins, although these drugs have been reported to inhibit prostaglandin synthesis in vitro and also were found to reduce the prostaglandin plasma levels in animals receiving these drugs. Another drug with low irritancy, meseclazone, markedly decreased both mucosal and plasma levels of prostaglandins. The results show that while ulcerogenic drugs reduce the mucosal and plasma prostaglandins levels in parallel with their ulcerogenicity, this relationship does not always hold for drugs with low ulcerogenic activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6953009&dopt=Abstract
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