OBJECTIVES: We developed a modified broncho-alveolar lavage (BAL) technique in order to perform repeated measurements of capillary-alveolar leakage of a macromolecule in oleic acid (OA)-induced lung injury. METHODS: BAL was performed in anesthetized dogs in a closed lung sampling site, using a bronchoscope fitted with an inflatable cuff. Fluorescein-labeled Dextran (FITC-D70) was continuously infused and its concentration measured in plasma and BAL fluid. A two-compartment model (blood and alveoli) was used to calculate K(AB), the transport-rate coefficient of FITC-D70 from blood to alveoli. K(AB) was estimated every 15 minutes over three hours. RESULTS: K(AB), close to zero at base-line both in control (n = 3) and in OA-injured lungs (n = 7), reached a peak in permeability 30 minutes after the induction of OA injury (K(AB) = 1.43 +/- 0.31 . 10(- 3) . minutes(- 1)), followed by a slow recovery. CONCLUSIONS: We conclude that this technique allows the monitoring of capillary-alveolar transport of macromolecules in in vivo experimental models. This monitoring may prove useful to study the mechanisms of the exudative stage of acute lung injury and to test therapies aimed at slowing the alveolar accumulation of plasma proteins and procoagulant factors that contribute to alveolar fibrosis.
OBJECTIVES: We developed a modified broncho-alveolar lavage (BAL) technique in order to perform repeated measurements of capillary-alveolar leakage of a macromolecule in oleic acid (OA)-induced lung injury. METHODS: BAL was performed in anesthetized dogs in a closed lung sampling site, using a bronchoscope fitted with an inflatable cuff. Fluorescein-labeled Dextran (FITC-D70) was continuously infused and its concentration measured in plasma and BAL fluid. A two-compartment model (blood and alveoli) was used to calculate K(AB), the transport-rate coefficient of FITC-D70 from blood to alveoli. K(AB) was estimated every 15 minutes over three hours. RESULTS: K(AB), close to zero at base-line both in control (n = 3) and in OA-injured lungs (n = 7), reached a peak in permeability 30 minutes after the induction of OA injury (K(AB) = 1.43 +/- 0.31 . 10(- 3) . minutes(- 1)), followed by a slow recovery. CONCLUSIONS: We conclude that this technique allows the monitoring of capillary-alveolar transport of macromolecules in in vivo experimental models. This monitoring may prove useful to study the mechanisms of the exudative stage of acute lung injury and to test therapies aimed at slowing the alveolar accumulation of plasma proteins and procoagulant factors that contribute to alveolar fibrosis.