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TY - JOUR. T1 - Early phase microvascular interactions in rat jejunum between nitric oxide and vasopressin following indomethacin administration. AU - László, F.. AU - Whittle, B. J R. PY - 1998. Y1 - 1998. N2 - The involvement of endogenous vasopressin in the actions of indomethacin following the concurrent administration of the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on acute intestinal microvascular permeability has been investigated in the rat. Administration of indomethacin (10 mg/kg, s.c.) or L-NAME (10 mg/kg, s.c.) alone did not affect jejunal and ileal vascular permeability after 1 h, as determined by the leakage of radiolabelled serum albumin. In contrast, when indomethacin (10 mg/kg, s.c.) was injected concurrently with L-NAME (2-10 mg/kg, s.c.), significant dose-dependent plasma leakage occurred in the jejunum. Pretreatment with L-arginine (300 mg/kg s.c.) 15 min prior to L-NAME prevented these changes in microvascular permeability. ...
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Mertens, W.C.; Bramwell, V.H.; Banerjee, D.; Gwadry-Sridhar, F.; al-Mutter, N.; Parhar, R.S.; Lala, P.K., 1993: Sustained oral indomethacin and ranitidine with intermittent continuous infusion interleukin-2 in advanced renal cell carcinoma
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Indomethacin is a nonsteroidal anti-inflammatory drug (NSAID) that exhibits antipyretic and analgesic properties. Its mode of action, like that of other anti-inflammatory drugs, is not known. However, its therapeutic action is not due to pituitary-adrenal stimulation.. Indomethacin is a potent inhibitor of prostaglandin synthesis in vitro. Concentrations are reached during therapy which have been demonstrated to have an effect in vivo as well. Prostaglandins sensitize afferent nerves and potentiate the action of bradykinin in inducing pain in animal models. Moreover, prostaglandins are known to be among the mediators of inflammation. Since indomethacin is an inhibitor of prostaglandin synthesis, its mode of action may be due to a decrease of prostaglandins in peripheral tissues. Indomethacin has been shown to be an effective anti-inflammatory agent, appropriate for long-term use in rheumatoid arthritis, ankylosing spondylitis, and osteoarthritis. Indomethacin affords relief of symptoms; it does ...
In their letter, Cold et al. claim that, during continuous intravenous indomethacin treatment, "the ICP-reducing effect is sustained and the increase in AVDO2, the jugular venous lactate and EEG are transitory" and that they "find a low mortality of 10% in indomethacin treated severe head injury." We have been unable to find the data supporting these statements. In the report by Jensen et al. [4] indomethacin was administered intravenously throughout a 7-h period. During this period, the decrease in global CBF and the increase in CavO sub 2 remained. At 7 h after of infusion, ICP seemed to have returned close to pretreatment level (28 +/- 3 mmHg vs. 25 +/- 11 mmHg). There is a lack of information regarding physiologic parameters in patients with severe head injuries when indomethacin infusion is continued beyond of a focal mass expanding lesion in pigs cannot rightly be transferred to the pathophysiological events of severe human head injury." Although this is obviously true, it seems to us that ...
Indometacin, a non-steroidal anti-inflammatory drug (NSAID), has similar mode of action when compared to other drugs in this group. Indometacin is a nonselective inhibitor of cyclooxygenase (COX) 1 and 2, the enzymes that participate in prostaglandin synthesis from arachidonic acid. Prostaglandins are hormone-like molecules normally found in the body, where they have a wide variety of effects, some of which lead to pain, fever, and inflammation. By inhibiting the synthesis of prostaglandins, indometacin can reduce pain, fever, and inflammation.[6]. Besides, indometacin has logarithmic acid dissociation constant pKa of 3 to 4.5. Since the physiologic body pH is well above the pKa range of indometacin, most of the indometacin molecules will be dissociated into ionised form, leaving very little unionised form of indometacin to cross a cell membrane. If the pH gradient across a cell membrane is high, most of the indometacin molecules will be trapped in one side of the membrane with higher pH. This ...
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Recent studies have demonstrated that wheat peptides protected rats against non-steroidal anti-inflammatory drugs-induced small intestinal epithelial cells damage, but the mechanism of action is unclear. In the present study, an indomethacin-induced oxidative stress model was used to investigate the effect of wheat peptides on the nuclear factor-κB(NF-κB)-inducible nitric oxide synthase-nitric oxide signal pathway in intestinal epithelial cells-6 cells. IEC-6 cells were treated with wheat peptides (0, 125, 500 and 2000 mg/L) for 24 h, followed by 90 mg/L indomethacin for 12 h. Wheat peptides significantly attenuated the indomethacin-induced decrease in superoxide dismutase and glutathione peroxidase activity. Wheat peptides at 2000 mg/L markedly decreased the expression of the NF-κB in response to indomethacin-induced oxidative stress. This study demonstrated that the addition of wheat peptides to a culture medium significantly inhibited the indomethacin-induced release of malondialdehyde and
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TY - JOUR. T1 - Influence of pyramid environment on the wound healing effects of dexamethasone and indomethacin - a comparative study. AU - Surekha, Kamath. PY - 2011/12/1. Y1 - 2011/12/1. N2 - Shapes and angles of The Great Pyramid of Egypt are balanced and renowned for their energy properties. Studies have proved that beneficial effects are found on human health in pyramidal environment. The present study was designed to determine the efficacy of dexamethasone and indomethacin on incision and dead space wound models in rats under the influence of pyramid environment. A wooden pyramid model fabricated locally was used for the study. The parameters chosen were breaking strength of incised wound, breaking strength of granulation tissue, hydroxyproline content and histology. The results showed that the dexamethasone and indomethacin slow down all phases of wound healing and the inhibitory action of dexamethasone on wound healing was stronger than that of indomethacin. Thus pyramid exposure ...
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In accordance with the present invention, the controlled release formulation contains coated pellets of indomethacin of only one type. The pellet releases indomethacin in both immediate and sustained release form. The immediate release indomethacin is rapidly absorbed from the stomach to provide a bolus dose of active agent. The sustained release indomethacin is gradually released over time to maintain the blood levels at effective concentrations for long periods of time.
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In the paper the relation between the changes of a functional condition of ileum, composition of its microflora and secretory activity of Paneth cells has been investigated. Administration of lincomycin led to a reduction of total of symbiotic bacteria and appearance of opportunistic microflora. Statistically insignificant changes of speed of transit of intestinal contents and damage of barrier function of an intestinal epithelium were noted. The intestinal epithelium was characterized by signs of inflammation. Administration of indomethacin and methotrexate led to significant changes of a functional state of a small intestine of rats. The speed of transit of intestinal contents following indomethacin administration increased by 30%, and, on the contrary, decreased by 90% following administration of methotrexate. The ability of epithelium of ileum to adsorb vital dye in both cases increased (by 32 and 51%, respectively) indicating the damage of barrier function. Thus there were significant ...
The putative role of prostaglandin E2 (PGE2) in suppressing rejection of the fetal allograft (resorption) in C3H/HeJ and CBA/J allopregnant mice was tested by administration of the prostaglandin synthesis inhibitors indomethacin (INDO) and acetylsalicylic acid (ASA). When the resorption rate was low, INDO fed at a dose of 15 micrograms/ml in drinking water after implantation had a slight augmenting effect when the endogenous resorption rate was , 30%, but had no effect when the endogenous rate was higher or when bacterial lipopolysaccharide (LPS) was given. ASA fed at 50 micrograms/ml had no augmenting effect and did not increase sensitivity to the abortogen LPS in either CBA/J (LPS sensitive) or C3H/HeJ (LPS resistant) mice. Both INDO and ASA fed to CBA/J mice significantly reduced endogenous PGE2 extractable from the uteri of hormonally pseudopregnant mice after deciduoma induction. Feeding INDO at doses up to 30 micrograms/ml from day 2.5 of pregnancy impaired but failed to completely block ...
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BACKGROUND AND PURPOSE Newborn cells may participate in repair following ischemic brain injury, but their survival and function may be influenced by inflammation. METHODS We investigated the effects of indomethacin, a nonsteroidal antiinflammatory drug, on the fate of newborn cells following transient focal ischemia. RESULTS Bromodeoxyuridine (BrdU)-labeled cells, including migrating neuroblasts, were observed in the neighboring striatum and overlying cortex 1 day poststroke. The density of BrdU+ cells labeled with doublecortin, nestin, glial fibrillary acidic protein, or NG2 was increased at 14 and 28 days. Indomethacin increased BrdU+ cells of all lineages and reduced microglial/monocyte activation. CONCLUSIONS Indomethacin enhanced the accumulation of newborn cells following stroke.
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