Objective: To evaluate the effect of lung protective ventilation strategy on pulmonary inflammatory response in acute respiratory distress syndrome (ARDS).
Methods: The ARDS rabbit model was duplicated by saline alveolar-lavage. The rabbits were divided into six groups: (1) normal control group (N group); (2) ARDS group (M group); (3) low-volume with best end-expiratory pressure (PEEP, A group) group: tidal volume (V(T)) 6 ml/kg, PEEP 2 cm H(2)O greater than the pressure of lower inflection point in pressure-volume curve (P(LIP)); (4) normal-volume with best PEEP group (B group): V(T) 6 ml/kg, and PEEP P(LIP) + 2 cm H(2)O; (5) low-volume with high PEEP group (C group): V(T) 6 ml/kg, and PEEP 15 cm H(2)O; and (6) high-volume with zero PEEP group (D group): V(T) 20 ml/kg. Lung wet/dry weight ratios (W/D) were recorded to evaluate lung injury. After 4 h of ventilation, lung homogenates were prepared to detect nuclear factor-kappaB (NF-kappaB) activity by electrophoretic mobility gel shift assay (EMSA), tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) levels by enzyme-linked immunosorbent assay (ELISA) and their mRNA expression by reverse transcriptase-polymerase chain reaction (RT-PCR). Myeloperoxidase (MPO) and malondialdehyde (MDA) in lung homogenates were also assessed.
Results: After 4 h ventilation, W/D in A group (5.6 +/- 1.1) were significantly lower than those in B group, C group and D group (6.6 +/- 0.8, 6.6 +/- 1.0, 6.9 +/- 1.0, all P < 0.05). But there was no difference between A group and M group (5.8 +/- 0.5). NF-kappaB activity was the highest in D group, and that in A group was 331 +/- 113, which was decreased significantly as compared with B, C and D groups (455 +/- 63, 478 +/- 74, 645 +/- 162, all P < 0.05). The mRNA expression of TNF-alpha and IL-10 and their concentrations in lung homogenates in A group were lower than those in B, C and D groups. In A group, the concentrations of MPO and MDA in lung homogenates were significantly lower than those in B, C and D groups.
Conclusion: Lung protective ventilation strategy can inhibit lung inflammation and may improve lung injury in ARDS, but low tidal volume with high PEEP may increase lung inflammation.