The effect of partial liquid ventilation on inflammatory response in piglets with acute lung injury induced by lipopolysaccharide

Abstract

To evaluate the effect of partial liquid ventilation (PLV) on pro-inflammatory and anti-inflammatory factors change in lipopolysaccharide (LPS)-induced piglets acute lung injury (ALI). Twelve Shanghai white piglets were randomly divided into mechanical ventilation (MV) group (n=6) and PLV group (n=6). 60 μg×kg(-1)×h(-1) LPS were intravenous infused continuously for 2 hours to induce ALI model. PLV model was set on the basis of the MV by endotracheal injection of perfluorodecalin (PFC, 10 mL/kg). The hemodynamic and respiratory parameters such as mechanics and arterial blood gas analysis were monitored at basic condition and after lung injury establishment (0, 1, 2, 4 hours). The serum levels of interleukin (IL-1β, IL-6, IL-8, IL-10) and tumor necrosis factor-α (TNF-α) were dynamically monitored by enzyme linked immunosorbent assay (ELISA). A lung injury score was used to quantify lung tissues change under light microscopic observations. Ventilation and oxygenation function were improved gradually after PFC endotracheal injection in PLV group, and there were significant difference compared with MV group at 4 hours [heart rate (HR): 144 ± 6 beats/min vs. 179 ± 9 beats/min, respiratory rate (RR): 58 ± 4 beats/min vs. 77 ± 6 beats/min, mean arterial blood pressure (MAP): 99 ± 7 mmHg vs. 75 ± 29 mmHg, dynamic lung compliance (Cdyn): 1.9 ± 0.3 mL×cmH(2)O(-1)×kg(-1) vs. 1.2 ± 0.4 mL×cmH(2)O(-1)×kg(-1), tidal volume (VT): 7.8 ± 0.4 mL/kg vs. 5.8 ± 0.9 mL/kg, mean airway resistance (Raw): 20.5 ± 6.6 cmH(2)O×L(-1)×s(-1) vs. 35.2 ± 4.0 cmH(2)O×L(-1)×s(-1), mean airway pressure (Paw): 1.0 ± 0.5 cmH(2)O vs. 3.0 ± 0.9 cmH(2)O, ventilation efficacy index (VEI): 0.18 ± 0.02 vs. 0.08 ± 0.02, pH value: 7.386 ± 0.143 vs. 7.148 ± 0.165, arterial partial pressure of oxygen (PaO(2)): 121.8 ± 12.5 mmHg vs. 73.6 ± 10.9 mmHg, arterial partial pressure of carbon dioxide (PaCO(2)): 39.6 ± 20.3 mmHg vs. 66.8 ± 23.5 mmHg, oxygenation index (PaO(2)/FiO(2)): 311 ± 35 mmHg vs. 184 ± 27 mmHg, P<0.05 or P<0.01]. All serum cytokines in both groups were significantly increased after LPS-induced ALI, and showed an elevated tendency. The serum pro-inflammatory factors of TNF-α, IL-1β, IL-6 and IL-8 in PLV group were significantly lower than those in MV group at 4 hours (TNF-α: 98.4 ± 21.1 ng/L vs. 178.0 ± 55.0 ng/L, IL-1β: 142.0 ± 38.0 ng/L vs. 226.0 ± 55.0 ng/L, IL-6: 763.0 ± 282.0 ng/L vs. 1 303.0 ± 260.0 ng/L, IL-8: 1 183.0 ± 403.0 ng/L vs. 1 876.0 ± 232.0 ng/L, P<0.05 or P<0.01). There was no significant difference in serum anti-inflammatory factor of IL-10 between PLV and MV groups at 4 hours (292.0 ± 40.0 ng/L vs. 208.0 ± 82.0 ng/L, P>0.05). The ratio of TNF-α/IL-10 in PLV group was significantly decreased compared with MV group at 2 hours (0.58 ± 0.13 vs. 1.13 ± 0.54, P<0.05). The ratio of IL-6/IL-10 in PLV group was significantly decreased compared with MV group at 4 hours (2.72 ± 1.27 vs. 7.17 ± 3.08, P<0.01). Microscopic changes in intra-alveolar and interstitial inflammation, hemorrhage and edema were better in PLV group than those in MV group. The lung injury score of PLV group was lower than MV group (independent lung regions: 9.8 ± 0.8 vs. 11.8 ± 1.0, t=3.956, P=0.003; dependent lung regions: 5.0 ± 0.6 vs. 14.7 ± 2.3, t=10.127, P=0.000). PLV can significantly reduce the levels of pro-inflammatory factors and the ratio of pro-inflammatory/anti-inflammatory factor, which may contribute to the protective effects of PLV on ALI.