• H Wu, T Kobayashi, Q Wan, W Shi, H Qian, X Cui, and W Li.
• Department of Anesthesiology, Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
• Acta Anaesthesiol Scand. 2010 Mar 1;54(3):354-61.

BackgroundOverdistension of the lung causes ventilator-induced lung injury (VILI) accompanied by surfactant abnormalities and inflammatory changes. We investigated the effects of surfactant replacement on overdistension of the terminal airspaces and plasma cytokine levels in VILI.MethodsVILI was induced by high-pressure ventilation (HPV) in rats anesthetized with pentobarbital, followed by ventilation for 2 h in the maintenance mode (tidal volume=10 ml/kg, positive end-expiratory pressure = 7.5 cmH(2)O) with or without surfactant replacement. The sizes of the terminal airspaces were determined after fixing the lungs at an airway pressure of 10 cmH(2)O on deflation. Cytokine levels were assessed by enzyme-linked immunosorbent assay.ResultsThe mean ratio of the largest terminal airspace size class (> or = 64,000 microm(2)) was increased from 13.4% to 32.0% by HPV (P<0.05). After maintenance-mode ventilation, the ratio decreased to 16.1% with surfactant replacement (P<0.05), but increased to 44.6% without surfactant replacement (P<0.05). Mean macrophage inflammatory protein-2 (MIP-2) levels in the plasma increased from <0.02 to 6.9 ng/ml with HPV (P<0.05), and further increased to > or = 11.8 ng/ml, regardless of surfactant replacement after maintenance-mode ventilation. Similar tendencies were observed in the interleukin (IL)-6 and IL-10 levels. Tumor necrosis factor-alpha levels were almost negligible during the experiment.ConclusionIn rats with VILI, surfactant replacement reversed overdistension of the terminal airspaces that may induce barotrauma, but not upregulation of MIP-2, IL-6, and IL-10 within 2 h.

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