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Effect of N-acetylcysteine on cardiopulmonary bypass-induced lung injury in dogs / 中华麻醉学杂志
Chinese Journal of Anesthesiology ; (12): 795-798, 2011.
Artículo en Chino | WPRIM | ID: wpr-422468
ABSTRACT
ObjectiveTo investigate the effect of N-acetylcysteine on lung injury induced by cardiopulmonary bypass(CPB) in dogs.MethodsThirty-six healthy adult mongrel dogs of both sexes weighing 15-16 kg were randomly assigned into 2 groups (n =18 each)CPB group (group C) and N-acetylcysteine group(group N).Lung injury was produced by CPB.In group N N-acetylcysteine 150 mg/kg was injected iv immediately before CPB,followed by infusion at 20 mg· kg-1 · h-1 until 60 min after termination of CPB.Blood samples were taken from femoral artery before CPB (T0,baseline),30 and 60 min after termination of CPB (T1,T2 ).Oxygenation index ( OI =PaO2 ÷ FiO2 ) and respiratory index (RI =PA-(a) DO2 ÷ PaO2 ) were calculated.Six animals were sacrificed at each time point.Lung specimens were obtained for microscopic examination,and determination of transforming growth factor-β1 (TGF-β1) mRNA expression,MDA content and SOD activity.ResultsCPB significantly increased RI,MDA content and TGF-β1 mRNA expression and decreased OI and SOD activity at T1 and T2 as compared with the baseline values at T0 in group C.N-acetylcysteine administered before and during CPB significantly attenuated CPB-induced above changes in OI,RI,MDA content,SOD activity and TGF-β1 mRNA expression.Microscopic examination showed that N-acetylcysteine significantly ameriorated CPB-induced lung damage.ConclusionsN-acetylcysteine administered before and during CPB can attenuate CPB-induced lung injury by inhibiting lipid peroxidation response and down-regulating TGF-β1 expression.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Anesthesiology Año: 2011 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Anesthesiology Año: 2011 Tipo del documento: Artículo