Continuous Renal Replacement Therapy Reduces the Systemic and Pulmonary Inflammation Induced by Venovenous Extracorporeal Membrane Oxygenation in a Porcine Model

Pulmonary changes in veno-venous extracorporeal membrane oxygenation (VV-ECMO) are rarely determined. We compared the contribution of VV-ECMO and cannulation based on the observation of pulmonary inflammatory reaction and parenchymal construction in a porcine model of low tidal volume (VT ) ventilation. We also evaluated the effect of adding continuous renal replacement therapy (CRRT) to the ECMO circuit, because CRRT is known to reduce systemic cytokine release induced by VV-ECMO. A total of 18 pigs undergoing low-VT ventilation were randomly divided into three groups (group 1, cannulation; group 2, VV-ECMO; group 3, VV-ECMO + CRRT) and studied for 24 h. Hemodynamic and ventilation parameters were recorded. We assessed plasma and alveolar cytokines, expression of pulmonary inflammatory genes, histopathological grading, and ultrastructural changes of the lungs. During the process, inspiratory volume increased and PaO2 decreased in group 1. Systemic tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) levels increased at 2 h in group 2 and partly decreased in group 3. At 24 h, the levels of bronchoalveolar lavage fluid, TNF-α, and IL-6 in group 2 were remarkably higher than those in groups 1 and 3. Pulmonary mRNA expression of cytokines did not differ between the groups. We observed an increased score of pulmonary pathological findings in pro-inflammatory cell infiltration and interstitial thickening of the lungs in group 2. The epithelium of the blood-air barrier after VV-ECMO was swollen. In group 3, the pulmonary parenchyma and blood-air barrier were well preserved. We concluded that in a porcine model of low-VT ventilation, both VV-ECMO and VV-ECMO in combination with CRRT provided adequate oxygenation and carbon dioxide removal. Compared with VV-ECMO alone, VV-ECMO in combination with CRRT better preserved the lung parenchyma by eliminating systemic cytokines.