Background: The energy delivered by a ventilator to the respiratory system in one minute is defined as mechanical power (MP). However, the effect of the ventilator-induced lung injury (VILI) in patients suffering of acute respiratory distress syndrome (ARDS) is still unknown. Our previous studies revealed that CXCL10 may be a potential biomarker of lung injury in ARDS. Therefore, the aim of this study was to compare the lung injury of rats and patients under different MP conditions to explore the involvement of CXCL10 and its receptor CXCR3 in VILI.
Methods: Patients were divided into high mechanical power group (HMP) and low mechanical power group (LMP), while rats were assigned to the high mechanical power group (HMP), medium mechanical power group (MMP) and low mechanical power group (LMP). CXCL10 and CXCR3 plasma content in ARDS patients and rats under ventilation at different MP was measured, as well as their protein and mRNA expression in rat lungs.
Results: CXCL10 and CXCR3 content in the plasma of ARDS patients in the HMP was significantly higher than that in the LMP. The increase of MP during mechanical ventilation in the rats gradually increased lung damage, and CXCL10 and CXCR3 level in rat plasma gradually increased with the increase of MP. CXCL10 and CXCR3 protein and mRNA expression in the HMP group and MMP group was significantly higher than that in the LMP group (P<0.05). More mast cells were present in the trachea, bronchus, blood vessels, and lymphatic system in the rat lungs of the HMP group and the number of mast cells in the HMP group (13.32±3.27) was significantly higher than that in the LMP group (3.25±0.29) (P＜0.05).
Conclusion: The higher the MP, the more severe the lung injury, the higher CXCL10/CXCR3 expression. Therefore, CXCL10/CXCR3 might participate in VILI by mediating mast cell chemotaxis.