Inhibition of nitro-oxidative stress attenuates pulmonary and systemic injury induced by high-tidal volume mechanical ventilation

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dc.contributor.author Martínez Caro, Leticia
dc.contributor.author Nin, Nicolás
dc.contributor.author Sánchez Rodríguez, Carolina
dc.contributor.author Ferruelo, A.
dc.contributor.author El-Assar, M.
dc.contributor.author Paula, Marta de
dc.contributor.author Fernández Segoviano, P.
dc.contributor.author Esteban, Andrés
dc.contributor.author Lorente Balanza, José Ángel
dc.date.accessioned 2016-12-22T15:56:32Z
dc.date.available 2016-12-22T15:56:32Z
dc.date.issued 2015
dc.identifier.citation Martínez-Caro, L., Nin, N., Sánchez-Rodríguez, C., Ferruelo, A., El Assar, M., de Paula, M., ... & Lorente, J. A. (2015). Inhibition of Nitro-Oxidative Stress Attenuates Pulmonary and Systemic Injury Induced by High–Tidal Volume Mechanical Ventilation. Shock, 44(1), 36-43. DOI: 10.1097/SHK.0000000000000381 spa
dc.identifier.issn 10732322
dc.identifier.uri http://hdl.handle.net/11268/6123
dc.description.abstract Mechanisms contributing to pulmonary and systemic injury induced by high tidal volume (VT) mechanical ventilation are not well known. We tested the hypothesis that increased peroxynitrite formation is involved in organ injury and dysfunction induced by mechanical ventilation. Male Sprague-Dawley rats were subject to low- (VT, 9 mL/kg; positive end-expiratory pressure, 5 cmH2O) or high- (VT, 25 mL/kg; positive end-expiratory pressure, 0 cmH2O) VT mechanical ventilation for 120 min, and received 1 of 3 treatments: 3-aminobenzamide (3-AB, 10 mg/kg, intravenous, a poly adenosine diphosphate ribose polymerase [PARP] inhibitor), or the metalloporphyrin manganese(III) tetrakis(1-methyl-4-pyridyl)porphyrin (MnTMPyP, 5 mg/kg intravenous, a peroxynitrite scavenger), or no treatment (control group), 30 min before starting the mechanical ventilation protocol (n = 8 per group, 6 treatment groups). We measured mean arterial pressure, peak inspiratory airway pressure, blood chemistry, and gas exchange. Oxidation (fluorescence for oxidized dihydroethidium), protein nitration (immunofluorescence and Western blot for 3-nitrotyrosine), PARP protein (Western blot) and gene expression of the nitric oxide (NO) synthase (NOS) isoforms (quantitative real-time reverse transcription polymerase chain reaction) were measured in lung and vascular tissue. Lung injury was quantified by light microscopy. High-VT mechanical ventilation was associated with hypotension, increased peak inspiratory airway pressure, worsened oxygenation; oxidation and protein nitration in lung and aortic tissue; increased PARP protein in lung; up-regulation of NOS isoforms in lung tissue; signs of diffuse alveolar damage at histological examination. Treatment with 3AB or MnTMPyP attenuated the high-VT mechanical ventilation-induced changes in pulmonary and cardiovascular function; down-regulated the expression of NOS1, NOS2, and NOS3; decreased oxidation and nitration in lung and aortic tissue; and attenuated histological changes. Increased peroxynitrite formation is involved in mechanical ventilation-induced pulmonary and vascular dysfunction. spa
dc.description.sponsorship SIN FINANCIACIÓN spa
dc.language.iso spa spa
dc.title Inhibition of nitro-oxidative stress attenuates pulmonary and systemic injury induced by high-tidal volume mechanical ventilation spa
dc.type article spa
dc.description.impact 3.048 JCR (2015) Q1, 33/200 Surgery; Q2, 12/33 Critical care medicine, 29/70 Hematology, 23/63 Peripheral vascular disease spa
dc.identifier.doi 10.1097/SHK.0000000000000381
dc.rights.accessRights closedAccess spa
dc.subject.uem Respiración spa
dc.subject.uem Aparato respiratorio spa
dc.subject.unesco Aparato respiratorio spa
dc.description.filiation UEM spa
dc.peerreviewed Si spa

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