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1 Groupe de Recherche en Physiopathologie Respiratoire et Unité des Soins Intensifs Médicaux, Département de Médecine, 3 Service d'inhalothérapie, Centre Hospitalier Universitaire de Sherbrooke, Quebec, Canada J1H 5N4; and 2 Unité de Toxicologie Industrielle et Médecine du Travail, Université Catholique de Louvain, 1200 Brussels, Belgium
After air-blood barrier injury, "pneumoproteins" specific to lung epithelial distal airspaces reaching the bloodstream are putative markers of lung hyperpermeability. The contribution of mechanical ventilation (MV) to this leakage is unknown. To explore this issue, 16-kDa Clara cell protein (CC-16) concentration was quantified in bronchoalveolar lavages (BALFs) and/or sera of rats first exposed either to ambient air or to 48 h of hyperoxia-induced acute lung injury and then ventilated for 2 h according to one of the following strategies: 1) spontaneous ventilation (SV), 2) very-low-volume high PEEP (VLVHP, where PEEP is positive end-expiratory pressure), 3) low-volume zero PEEP, 4) moderate-volume low PEEP, and 5) high-volume zero PEEP (HVZP). Results show that total proteins in BALFs increased with time and MV, with little impact from hyperoxia preexposure. CC-16 content decreased in BALFs but increased in the bloodstream during MV, suggesting intravascular leakage. Lung overdistension may result either from high-volume (HVZP) or high-PEEP (VLVHP) MV, and it was the most potent inducer of CC-16 leakage (P < 0.05 vs. SV). In the VLVHP group, pretreatment with keratinocyte growth factor was efficient in reducing blood CC-16 transfer.
acute lung injury/acute respiratory distress syndrome; ventilation-induced lung injury; 16-kDa Clara cell; keratinocyte growth factor; pneumoproteinemia
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