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Articles in PresS, published online ahead of print October 25, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00384.2001
Submitted on September 28, 2001
Accepted on October 21, 2002
1 Departement de Medecine, CHU de Sherbrooke, Sherbrooke, Quebec, Canada
2 Unite de toxicologie industrielle et Medecine du travail, Universite Catholique de Louvain, Bruxelles, Belgium
3 Service d'inhalotherapie, CHU de Sherbrooke, Sherbrooke, Quebec, Canada
* To whom correspondence should be addressed. E-mail: Olivier.Lesur{at}USherbrooke.ca.
Following 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, Clara Cell protein (CC-16) concentration was quantified in BALFs and/or sera of rats firstly exposed either to ambient air or to 48hr-hyperoxia-induced ALI, and then ventilated for 2hrs according to one of the following strategies : i) spontaneous ventilation (SV), ii) very low volume high PEEP (VLVHP), iii) low volume zero PEEP (LVZP), iv) moderate volume low PEEP (MVLP), and v) high volume zero PEEP (HVZP). Results show that total proteins in BALFs increased with time and MV, with little impact from hyperoxia pre-exposure. CC-16 content decreased in BALFs but increased in 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 (KGF) was efficient in reducing blood CC-16 transfer.
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