ArticleThe American journal of pathology2003
Functional significance of inducible nitric oxide synthase induction and protein nitration in the thermally injured cutaneous microvasculature.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Protective effect of snail secretion filtrate against ethanol-induced gastric ulcer in mice.Scientific reports · 2021Article
- Targeting the NO/superoxide ratio in adipose tissue: relevance to obesity and diabetes management.British journal of pharmacology · 2017Review
- Liver sinusoidal endothelial cells link hyperinsulinemia to hepatic insulin resistance.Diabetes · 2013Article
- Gamma delta (γδ) T-cells are critical in the up-regulation of inducible nitric oxide synthase at the burn wound site.Cytokine · 2012Article
- Article
- Gammadelta T-cells: potential regulators of the post-burn inflammatory response.Burns : journal of the International Society for Burn Injuries · 2009Review
- Bench-to-bedside review: Burn-induced cerebral inflammation--a neglected entity?Critical care (London, England) · 2009Review
- Article
- Poly (adp-ribose) synthetase inhibition reduces oxidative and nitrosative organ damage after thermal injury.Pediatric surgery international · 2005Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased nitric oxide (NO) production after burn injury is well established. However, there is little information relating to the reactions that occur as a consequence of NO generation under such circumstances. We have investigated the synthesis and function of NO in a rat model of local cutaneous thermal injury. We show that NO levels are elevated from 3 hours after injury with a concomitant increase in protein nitration. A selective inducible nitric oxide synthase (iNOS) inhibitor (1400W) significantly attenuated NO synthesis, protein nitration, and neutrophil accumulation in this model, but had no effect on edema formation. The results also indicate that NO synthesis and protein nitration occurred independently of neutrophil accumulation because these parameters were unaffected by depletion of circulating neutrophils. 3-Chlorotyrosine, a marker of neutrophil/myeloperoxidase-mediated protein damage was significantly increased from 1 hour after burn. Our observations provide evidence for the involvement of reactive species in the inflammatory response after burn. The use of selective iNOS inhibitors may represent a novel approach for the management of human burn injuries.
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Registered trials
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