PEAK End-Tidal NO as a biomarker for investigating the effect of different OLV strategies on lung injury and inflammation response.

Abstract

Abstract One-lung ventilation (OLV) aggravates alveolar damage and inflammation response in the lung. The evaluation indicators of lung injury caused by OLV are not perfect. End-tidal fraction of nitric oxide (ETNO) continuously collected during ventilation may be a new and non-invasive inflammatory marker of lung injury to investigate the effect of different OLV strategies. A total of 56 patients undergoing thoracic surgery were included and randomized into two groups. These patients had the same parameters during two-lung ventilation, but during OLV, the High-Volume group was set at a tidal volume (VT)=8 ml/kg predicted body weight (PBW) and a positive end-expiratory pressure (PEEP)=5 cmH2O, while the Low-Volume group was set at a VT=5 ml/kg PBW and a PEEP=5 cmH2O with recruitment every 30 min. ETNO was acquired at the points of induction, OLV 0 min, OLV 15 min, OLV 30 min, OLV 1 h and immediately at two-lung re-ventilation. We also obtained traditional evaluation indicators at the same points. ETNO did not differ significantly between groups at baseline. When the patients suffered OLV, compared with the Low-Volume group, ETNO in the High-Volume group significantly decreased at all points (P<0.001), and the expression of endothelial NO synthase in plasma decreased but lagged for a quarter. There was almost no change in traditional inflammatory factor in plasma. Compared with traditional inflammatory factor, ETNO can be a new, rapid, convenient and accurate inflammatory marker for investigating the effects of different OLV strategies in early-phase lung injury and pro-inflammation response. Clinical trial registration.ChiCTR1800015993