Oxygenation, inflammatory response and lung injury during one lung ventilation in rabbits using inspired oxygen fraction of 0.6 vs. 1.0

Abstract

Maintaining adequate oxygenation during one-lung ventilation (OLV) requires high inspired oxygen fraction (FiO2). However, high FiO2 also causes inflammatory response and lung injury. Therefore, it remains a great interest to clinicians and scientists to optimize the care of patients undergoing OLV. The aim of this study was to determine and compare oxygenation, inflammatory response and lung injury during OLV in rabbits using FiO2 of 0.6 vs. 1.0. After 30 minutes of two-lung ventilation (TLV) as baseline, 30 rabbits were randomly assigned to three groups receiving mechanical ventilation for 3 hours: the sham group, receiving TLV with 0.6 FiO2; the 1.0 FiO2 group, receiving OLV with 1.0 FiO2; the 0.6 FiO2 group, receiving OLV with 0.6 FiO2. Pulse oximetry was continuously monitored and arterial blood gas analysis was intermittently conducted. Histopathologic study of lung tissues was performed and inflammatory cytokines and the mRNA and protein of nuclear factor kappa B (NF-κB) p65 were determined. Three of the 10 rabbits in the 0.6 FiO2 group suffered hypoxemia, defined by pulse oximetric saturation (SpO2) less than 90%. Partial pressure of oxygen (PaO2), acute lung injury (ALI) score, myeloperoxidase (MPO), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), mRNA and protein of NF-κB p65 were lower in the 0.6 FiO2 group than in the 1.0 FiO2 group. In conclusion, during OLV, if FiO2 of 0.6 can be tolerated, lung injury associated with high FiO2 can be minimized. Further study is needed to validate this finding in human subjects.

A randomized controlled trial of positive end-expiratory pressure on pulmonary oxygenation and biventricular function in esophageal cancer patients receiving one-lung ventilation under a lower FiO2

“…Previous studies showed hyperoxia during OLV increased the levels of inflammation and oxidative stress, leading to a higher risk of complications after surgery ( 21 , 22 ). Our previous research studied the benefits of lower FiO 2 in lowering inflammation, oxidative stress, and lung injury ( 8 , 9 ). Although higher PEEP increased oxygenation, the levels of inflammation also increased.…”

“…Although high fraction of inspiration O 2 (FiO 2 ) (1.0) improved oxygenation ( 5 ), the following higher levels of inflammation remarkably raised acute respiratory distress syndrome (ARDS) risk, leading to increased postoperative mortality ( 6 , 7 ). Several reports have shown the independent risk factors for ARDS are high FiO 2 and airway pressure, as well as prolonged OLV ( 6 - 8 ), and maximizing the use of minimum FiO 2 under adequate oxygenation is the current recommended strategy for protective ventilation ( 3 ).…”

“…Our previous animal study has shown low FiO 2 (0.6) could produce less inflammation, oxidative stress, and lung injury than FiO 2 (1.0) after OLV [positive end-expiratory pressure (PEEP) =0 cmH 2 O, VT =10 mL/kg] ( 8 ). However, 30% (3/10) of animals developed hypoxemia and required elevated FiO 2.…”

Metastasis-Associated 1 (MTA1) Gene Expression Promotes Angiogenesis in Mouse Xenografts from Human Non-Small Cell Lung Cancer (NSCLC) Cells

“…MTA1 is part of the nuclear remodeling and deacetylation (NuRD) complex that ubiquitously regulates the expression of genes that enhance the migration and invasion of malignant cells [7]. Upregulation of MTA1 has been reported in a variety of cancers, including colorectal carcinoma [8,9], gastric cancer [10], and laryngeal squamous carcinoma [11]. In lung cancer, MTA1 has recently been identified as a prognostic biomarker that is associated with the poor prognosis in patients with lung cancer [12,13].…”

Protective effects of dexmedetomidine on lung in rats with one‑lung ventilation

“…Hypoventilation may cause hypoxia and ischemic damage and destruction of cells. In the process of restoring blood supply, it can also increase the damage of cells, cause pathological and physiological changes in the lungs, and induce ischemia-reperfusion injury, and hypoxemia followed by acute inflammatory reactions and oxidative stress reactions, causing acute injury to multiple organs throughout the body (3,4). Studies have shown that prolonged OLV and mechanical stimuli resulting from surgery can lead to the activation of inflammatory cells in patients, and the release of inflammatory factors may cause increased inflammatory reactions in the lungs and increased lung injury in patients, which in turn increase the risk of postoperative death (5).…”