• J Gorrasi, G Peluffo, H Botti, C Batthyany, M Naviliat, E Barrios, H Correa, and R Radi.
• Departamento de Emergencia, Hospital de Clínicas, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay; Centro de Tratamiento Intensivo, Hospital de Clínicas, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay; Center for Free Radical and Biomedical Research (CEINBIO), Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. Electronic address: jgorrasi@hc.edu.uy.
• J Crit Care. 2019 Jun 1; 51: 204-212.

PurposeDuring sepsis and mechanical ventilation oxidative stress is generated by endothelial and inflammatory lung cells. Our main objective was to study pulmonary NO (nitric oxide) production and nitroxidative stress in mechanically-ventilated septic patients.MethodsWe study 69 mechanically ventilated patients, 36 with sepsis and 33 without sepsis within the first 48 h of ICU admission compared with 33 mechanically ventilated patients without sepsis (MV) plus eight operating room patients without lung disease served as control healthy group (ORCG). Nitrite plus nitrate (NOx-), 3-nitrotyrosine and malondialdehyde (MDA) in bronchoalveolar lavage fluid (BALF) were analyzed.ResultsBALF NOx-, BALF 3-nitrotyrosine, BALF MDA, and plasma NOx- were higher in the Sepsis than in MV patients (all p < .05). Both SG and MV patients had higher BALF NOx- than the healthy control group (p < .001). In the Sepsis patients, the ICU non-survivors had higher levels of BALF NOx- than ICU survivors 80(70-127) μM versus 31(15-47) μM, p < .001.ConclusionsWe conclude that during early phases of sepsis there is an enhanced lung nitroxidative stress due to an increase of NO production leading to secondary NO-derived oxidants, which promote protein nitration and lipid peroxidation.Copyright © 2019. Published by Elsevier Inc.

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