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dc.contributor.authorSuborov, Evgeny
dc.contributor.authorSmetkin, Alexey Anatolievich
dc.contributor.authorKondratyev, Timofey
dc.contributor.authorValkov, Andrey Yurjevich
dc.contributor.authorKuzkov, Vsevolod
dc.contributor.authorKirov, Mikhail
dc.contributor.authorBjertnæs, Lars J.
dc.date.accessioned2013-03-07T09:29:16Z
dc.date.available2013-03-07T09:29:16Z
dc.date.issued2012
dc.description.abstractMechanical ventilation with high tidal volumes may cause ventilator-induced lung injury (VILI) and enhanced generation of nitric oxide (NO). We demonstrated in sheep that pneumonectomy followed by injurious ventilation promotes pulmonary edema. We wished both to test the hypothesis that neuronal NOS (nNOS), which is distributed in airway epithelial and neuronal tissues, could be involved in the pathogenesis of VILI and we also aimed at investigating the influence of an inhibitor of nNOS on the course of VILI after pneumonectomy. Anesthetized sheep underwent right pneumonectomy, mechanical ventilation with tidal volumes (VT) of 6 mL/kg and FiO2 0.5, and were subsequently randomized to a protectively ventilated group (PROTV; n = 8) keeping VT and FiO2 unchanged, respiratory rate (RR) 25 inflations/min and PEEP 4 cm H2O for the following 8 hrs; an injuriously ventilated group with VT of 12 mL/kg, zero end-expiratory pressure, and FiO2 and RR unchanged (INJV; n = 8) and a group, which additionally received the inhibitor of nNOS, 7-nitroindazole (NI) 1.0 mg/kg/h intravenously from 2 hours after the commencement of injurious ventilation (INJV + NI; n = 8). We assessed respiratory, hemodynamic and volumetric variables, including both the extravascular lung water index (EVLWI) and the pulmonary vascular permeability index (PVPI). We measured plasma nitrite/nitrate (NOx) levels and examined lung biopsies for lung injury score (LIS). Both the injuriously ventilated groups demonstrated a 2–3-fold rise in EVLWI and PVPI, with no significant effects of NI. In the INJV group, gas exchange deteriorated in parallel with emerging respiratory acidosis, but administration of NI antagonized the derangement of oxygenation and the respiratory acidosis significantly. NOx displayed no significant changes and NI exerted no significant effect on LIS in the INJV group. Inhibition of nNOS improved gas exchange, but did not reduce lung water extravasation following injurious ventilation after pneumonectomy in sheep.en
dc.identifier.citationBMC Anesthesiology 12(2012) nr. 10en
dc.identifier.cristinIDFRIDAID 973082
dc.identifier.doihttp://dx.doi.org/10.1186/1471-2253-12-10
dc.identifier.issn1471-2253
dc.identifier.urihttps://hdl.handle.net/10037/4889
dc.identifier.urnURN:NBN:no-uit_munin_4605
dc.language.isoengen
dc.publisherBioMed Centralen
dc.rights.accessRightsopenAccess
dc.subjectVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Lung diseases: 777en
dc.subjectVDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Lungesykdommer: 777en
dc.titleInhibitor of neuronal nitric oxide synthase improves gas exchange in ventilator-induced lung injury after pneumonectomy.en
dc.typeJournal articleen
dc.typeTidsskriftartikkelen
dc.typePeer revieweden


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