naproxen-n-butyl-nitrate and Enteritis
naproxen-n-butyl-nitrate has been researched along with Enteritis* in 2 studies
Reviews
1 review(s) available for naproxen-n-butyl-nitrate and Enteritis
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Nitric oxide-modulating agents for gastrointestinal disorders.
Almost 20 years after the identification of the biological role of nitric oxide (NO), the full therapeutic potential of novel agents that mimic the activity of NO or interfere with its synthesis has yet to be realised for utilities involving the gastrointestinal tract. New utilities for classical NO donors, which were used as vasodilators for decades, in the treatment of motility disorders have been explored and a product for treating anal fissure was recently launched. New classes of compounds incorporating a NO-donating moiety into standard non-steroidal anti-inflammatory drugs, the NO-non-steroidal anti-inflammatory drugs (NO-NSAIDs) or COX-inhibiting nitric oxide donors (CINODs) have also been developed. These have been shown to exhibit reduced gastrointestinal injury in experimental models, and reports on their efficacy and safety in Phase I and II studies are now available. Modulation of the inducible NO synthase isoform that generates excessive NO that can lead to subsequent cytotoxic moieties, such as peroxynitrite, may have therapeutic possibilities in a range of inflammatory diseases of the gut. Likewise, agents that promote the decomposition of peroxynitrite or removal of its other component, superoxide, may also prove to be of use. Further targets for pharmaceutical exploitation are likely to come from both genomic and molecular insights into the processes that regulate the NO system. Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Enteritis; Esophagus; Fissure in Ano; Gastric Emptying; Gastrointestinal Diseases; Gastrointestinal Motility; Humans; Naproxen; Nitrates; Nitric Oxide; Nitric Oxide Donors; Nitric Oxide Synthase Type II; Peroxynitrous Acid | 2005 |
Other Studies
1 other study(ies) available for naproxen-n-butyl-nitrate and Enteritis
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The effects of AZD3582 [4-(nitroxy)butyl-(2S)-2-(6-methoxy-2-naphthyl) propanoate], and naproxen on key pathogenic steps in NSAID-enteropathy in the rat.
The pathogenesis of NSAID-induced enteropathy may involve dual inhibition of the cyclooxygenase (1 and 2) and a topical effect with sequential increased intestinal permeability, development of inflammation and ulcers. It has been suggested that nitric-oxide donating drugs cause significantly less gastrointestinal injury by counteracting for NSAID-induced reductions in blood flow.. To compare the effects of AZD3582 [4-(nitroxy)butyl-(2S)-2-(6-methoxy-2-naphthyl) propanoate], and naproxen on key pathogenic steps in NSAID-enteropathy in the rat.. Single doses of AZD3582, naproxen (dose range 10-300 micromol/kg) or vehicle were given to male Sprague Dawley rats. Intestinal permeability (51CrEDTA) and intestinal inflammation (granulocyte marker protein) was quantitated and ulcer counts made.. Intestinal permeability (all doses) and inflammation (highest dose of the drugs) increased significantly from control levels following naproxen and AZD3582 and there was no significant difference between the drugs. Median ulcer counts were, however, significantly (p < 0.01) lower with AZD3582 (4 +/- 2) than with naproxen (17 +/- 4).. Naproxen and AZD3582 are equally associated with increased small intestinal permeability and inflammation, which is the consequence of their topical effect. The reduced small bowel ulcer counts with AZD3582 accords with the suggestion that vascular factors are the main driving force for NSAID-induced ulcer formation. Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Enteritis; Intestinal Diseases; Male; Naproxen; Nitric Oxide Donors; Permeability; Rats; Rats, Sprague-Dawley; Ulcer | 2007 |