Plasma Lipidomics Identify Pathways Linked to Acute Lung Injury in a Porcine One-Lung Ventilation Surgery Model

Area of Science:

• Anesthesiology and Perioperative Medicine
• Pulmonary Medicine
• Biochemistry and Metabolism

Background:

• One-lung ventilation (OLV) is crucial for thoracic surgery but can lead to postoperative lung injury.
• Lung-protective ventilation (LPV) strategies are recommended, but preventing hypoxemia may necessitate higher fraction of inspired oxygen (FiO2) or tidal volumes (VT).
• The impact of these ventilation strategies on pro-inflammatory lipid mediators remains unclear.

Purpose of the Study:

• To investigate whether high FiO2 or VT during OLV contributes to elevated pro-inflammatory lipid mediators postoperatively.
• To compare the effects of normoxic LPV, hyperoxic LPV, and injurious mechanical ventilation (IMV) on lipid profiles.
• To identify specific lipid biomarkers associated with lung injury during OLV.

Main Methods:

• A porcine model underwent left upper lobectomy requiring OLV.
• Pigs were randomized into three groups: LPV-NO (normoxic, low VT), LPV-HO (hyperoxic, low VT), and IMV (normoxic, high VT).
• Arterial plasma was analyzed using LC-MS/MS for lipidomic profiling before and after OLV.

Main Results:

• Hyperoxic LPV (LPV-HO) significantly increased lysophosphatidylethanolamines, free fatty acids, phosphatidylserine, lysophosphatidylcholine, triglycerides, and phosphatidylethanolamines.
• Injurious mechanical ventilation (IMV) significantly increased triglycerides, diglycerides, linoleyl-carnitine, and free fatty acids.
• Normoxic LPV (LPV-NO) did not result in significant changes in lipid biomarker levels post-surgery.

Conclusions:

• Both high FiO2 and high VT during OLV contribute to systemic lipid metabolic derangements.
• Elevated lipids in LPV-HO and IMV groups are linked to inflammatory pathways involved in lung injury.
• Targeting these lipid pathways intraoperatively may offer a strategy to mitigate postoperative pulmonary complications.