Effect of lung protective ventilation strategy on pulmonary inflammatory response in acute respiratory distress syndrome (ARDS) rabbit model

Objective

To evaluate the effect of lung protective ventilation strategy on pulmonary inflammatory response in ARDS.

Methods

The ARDS rabbits model were duplicated by saline alveoli-lavaged. The rabbit were divided into six groups: (1) normal; (2) ARDS; (3) low-volume with best positive end expiratory pressure (PEEP) (A) (tidal volume [VT] 6 ml/kg, PEEP 2 cmH₂O greater than the pressure of lower inflection point in pressure–volume curve [PLIP]); (4) normal volume with best PEEP (B) (VT 6 ml/kg, PEEP PLIP + 2 cm₂HO); (5) low volume with high PEEP (C) (VT 6 ml/kg, PEEP 15 cmH₂O); (6) high volume with zero PEEP (D) (VT 20 ml/kg). Lung wet/dry weight ratios (W/D) were recorded to assess lung injury. After 4 hours of ventilation, lung homogenates were prepared to detect NF-κB activity by EMSA, TNFα and IL-10 levels by ELISA and their mRNA expression by RT-PCR. Meanwhile MPO and MDA in lung homogenates were assessed.

Results

After 4 hours ventilation, W/D in group A (5.58 ± 1.05) were lower than groups B, C and D, significantly (6.56 ± 0.82, 6.58 ± 0.96, 6.94 ± 0.98, P < 0.05), but there was no difference between group A and the ARDS group. NF-κB activity was the highest in group D. NF-κB activity in group A was 331 ± 113, which was decreased significantly as compared with groups B, C and D (455 ± 63, 478 ± 74, 645 ± 162, P < 0.05). The mRNA expression of TNFα and IL-10 and their concentration in lung homogenates in group A was lower than groups B, C and D. In group A, the concentrations of MPO and MDA in lung homogenates were lower significantly than in groups B, C and D.

Conclusions

Lung protective ventilation strategy can inhibit the pulmonary inflammation and may improve lung injury in ARDS, but low low tidal volume with high PEEP may increase the lung inflammation.