ArticleBurns : journal of the International Society for Burn Injuries2011
Mechanistic aspects of inducible nitric oxide synthase-induced lung injury in burn trauma.
Article in Burns : journal of the International Society for Burn Injuries, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 15 citations in OpenAlex.
- Emerging therapies for smoke inhalation injury: a review.Journal of translational medicine · 2020Review
- R-100 improves pulmonary function and systemic fluid balance in sheep with combined smoke-inhalation injury and Pseudomonas aeruginosa sepsis.Journal of translational medicine · 2017Article
- Down-regulation of toll-like receptor 4 alleviates intestinal ischemia reperfusion injury and acute lung injury in mice.Oncotarget · 2017Article
- OXIDATIVE STRESS IN A RAT MODEL OF COTTON SMOKE INHALATION-INDUCED PULMONARY INJURY.African journal of traditional, complementary, and alternative medicines : AJTCAM · 2016Article
- Effects of basic drugs on prognosis of acute lung injury in mice.International journal of clinical and experimental medicine · 2015Article
- ROS-Mediated NLRP3 Inflammasome Activity Is Essential for Burn-Induced Acute Lung Injury.Mediators of inflammation · 2015Article
- Article
- Lung [(18)F]fluorodeoxyglucose uptake and ventilation-perfusion mismatch in the early stage of experimental acute smoke inhalation.Anesthesiology · 2014Article
- Optimal management of the critically ill: anaesthesia, monitoring, data capture, and point-of-care technological practices in ovine models of critical care.BioMed research international · 2014Review
- The role of iNOS inhibitors on lung injury induced by gastrointestinal decontamination agents aspiration.Journal of molecular histology · 2012Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
introductionAlthough the beneficial effects of inducible nitric oxide synthase (iNOS) inhibition in acute lung injury secondary to cutaneous burn and smoke inhalation were previously demonstrated, the mechanistic aspects are not completely understood. The objective of the present study is to describe the mechanism(s) underlying these favourable effects. We hypothesised that iNOS inhibition prevents formation of excessive reactive nitrogen species and attenuates the activation of poly(ADP) (poly(adenosine diphosphate)) ribose polymerase, thus mitigating the severity of acute lung injury in sheep subjected to combined burn and smoke inhalation.
methodsAdult ewes were chronically instrumented for a 24-h study and allocated to groups: sham: not injured, not treated, n = 6; control: injured, not treated, n = 6; and BBS-2: injured treated with iNOS dimerisation inhibitor BBS-2, n = 6. Control and BBS-2 groups received 40% total body surface area 3rd-degree cutaneous burn and cotton smoke insufflation into the lungs under isoflurane anaesthesia.
resultsTreatment with iNOS inhibitor BBS-2 significantly improved pulmonary gas exchange (partial pressure of oxygen in the blood/fraction of inspired oxygen (PaO₂/FiO₂) 409 ± 43 mmHg vs. 233 ± 50 mmHg in controls, p < 0.05) and reduced airway pressures (peak pressure 20 ± 1 cm H₂O vs. 28 ± 2 cm H₂O in controls, p < 0.05) and lung water content (lung wet-to-dry ratio 4.1 ± 0.3 vs. 5.2 ± 0.2 in controls, p < 0.05) 24h after the burn and smoke injury. BBS-2 significantly reduced the increases in lung lymph nitrite/nitrate (10 ± 3 μM vs. 26 ± 6 μM in controls, p < 0.05) and 3-nitrotyrosine (109 ± 11 (densitometry value) vs. 151 ± 18 in controls, p < 0.05). Burn/smoke-induced increases in lung tissue nitrite/nitrate, poly(ADP)ribose polymerase, nuclear factor-κB (NF-κB) activity, myeloperoxidase activity and malondialdehyde formation and interleukin (IL)-8 expression were also attenuated with BBS-2.
conclusionsThe results provide strong evidence that BBS-2 ameliorated acute lung injury by inhibiting the inducible nitric oxide synthase/reactive nitrogen species/poly(ADP-ribose) polymerase (iNOS/RNS/PARP) pathway.
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