Drugs online research references
J Gastroenterol Hepatol. 1992 Nov-Dec;7(6):586-90.
Adaptation of rat gastric mucosa to repeated doses of non-salicylate non-steroidal anti-inflammatory drugs.
Skeljo MV, Giraud AS, Yeomans ND.
University of Melbourne Department of Medicine, Western Hospital, Footscray, Victoria, Australia.
To determine whether gastric mucosal adaptation occurs to the damaging effects of repeated non-steroidal anti-inflammatory drug (NSAID) administration, we compared the extent of gastric damage in rats after single or repeated doses of four non-salicylate NSAID. With daily dosing, adaptation occurred only to repeated doses of the short-acting NSAID ibuprofen and diclofenac but not to indomethacin and naproxen, both of which have considerably longer half-lives. Adaptation to indomethacin was demonstrable if the dosage interval was lengthened and the drug was given on alternate days rather than daily. Histological examination of the gastric mucosa of diclofenac-treated rats showed a similar degree of superficial damage in the single and repeatedly dosed groups. However there was a highly significant reduction in the amount of deeper mucosal damage in the repeatedly dosed rats. Our findings show that under certain conditions of dosage, adaptation to non-salicylate NSAID is demonstrable. The pharmacokinetics of individual NSAID appear to be important in determining whether or not adaptation occurs. Histological examination showed that adaptation to one of the shorter acting NSAID, diclofenac, was characterized by a significant reduction in deeper mucosal damage.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1486187&dopt=Abstract
Dig Dis Sci. 2001 Feb;46(2):338-44.
Diclofenac-induced gastric mucosal fluorescence in rats.
Matsui H, Murata Y, Kobayashi F, Shiba R, Momo K, Kondo Y, Nakahara A, Muto H.
Division of Gastroenterology, Institute of Clinical Medicine, University of Tsukuba, Japan.
We previously reported that the gastric mucosa emits fluorescence of porphyrins at the onset of gastric lesions induced by hemorrhagic shock. In this study, we investigated whether the fluorescent substance concerns with the gastric mucosal injuries induced by diflofenac, a nonsteroidal antiinflammatory drug (NSAID). In the gastric mucosa treated with diclofenac, lesions were generated and myeloperoxidase activity increased. Diclofenac administration also increased thiobarbituric acid-reactive substances, a index of tissue peroxidation. After diclofenac treatment, the gastric mucosal fluorescence intensities rose. HPLC analysis demonstrated that the fluorescent substances were mesoporphyrin and protoporphyrin, which were the same as found in hemorrhagic shock. Pretreatment of the tissue with radical scavenging substances, catalase and troxipide, restrained the increase of mucosal fluorescence intensity, tissue peroxidation, and lesion formation. These findings indicate that diclofenac treatment induced the generation of porphyrins as well as tissue peroxidation in gastric mucosal tissue. This study suggests that autofluorescence observation is a useful tool to identify diclofenac-induced gastric injury.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11281183&dopt=Abstract
Prostaglandins Leukot Essent Fatty Acids. 1992 Jul;46(3):175-82.
Papaverine effects on PGI2 and TXA2 release from the canine vascular wall.
Brunkwall JS, Stanley JC, Jackson T, Andersson D, Bergqvist D.
Department of Surgery, Lund University, Malmo General Hospital, Sweden.
Operative manipulation of blood vessels might lead to spasm, thereby destroying the endothelial cell function: the spasm can be prevented by the vasodilator papaverine. To study if this was mediated via the prostanoid pathway the following investigation was undertaken: canine jugular veins and carotid arteries were dissected with or without papaverine. Vessel segments were then perfused with Hank's balanced salt solution for five times 15 min. Prostacyclin was measured as the stable degradation product 6-keto-PGF1 alpha and thromboxane as TXB2, by radioimmunoassay. Control arterial segments' 6-keto-PGF1 alpha release was initially 129.5 + 20.1 pg/mm2/15 min, and 29.7 + 10.4 after 60 min (p less than 0.05 vs initial value) and responded to arachidonic acid (AA) with an increase to 139.2 +/- 23.1 pg/mm2/15 min (p less than 0.05). Segments treated with papaverine had the same release as the controls. In venous segments there was a lower initial release (p less than 0.05) from segments given papaverine than from controls, but this was more likely an effect of papaverine on the assay. There was no difference in release of prostacyclin from segments given papaverine in the perfusate compared to controls when using 125I tracer. When using 3H tracer including absorption of free antigen to dextran coated charcoal, papaverine displaced the free tracer giving artificially low values. There was no effect of papaverine given intraoperatively on the TXB2 release, neither from arteries nor from veins. In another experiment the vessel wall tension was examined and the cyclooxygenase inhibitor diclofenac did not inhibit the vasodilating effect of papaverine.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1508951&dopt=Abstract
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