Research Increased cardiac index due to terbutaline treatment aggravates capillary-alveolar macromolecular leakage in oleic acid lung injury

摘要: Introduction We assessed the in vivo effects of terbutaline, a beta2-agonist assumed to reduce microvascular permeability acute lung injury. Methods used recently developed broncho-alveolar lavage (BAL) technique repeatedly measure (every 15 min. for 4 hours) time-course capillary-alveolar leakage macromolecule (fluorescein-labeled dextran) 19 oleic acid (OA) injured dogs. BAL was performed closed sampling site, using bronchoscope fitted with an inflatable cuff. Fluorescein-labeled Dextran (FITC-D70) continuously infused and its concentration measured plasma fluid. A two-compartment model (blood alveoli) calculate KAB, transport rate coefficient FITC-D70 from blood alveoli. KAB estimated every minutes over hours. Terbutaline intra-venous perfusion started 90 after onset injury then until end experiment. Results In non-treated group, reached peak within 30 OA Thereafter decreased gradually infusion, min injury, interrupted recovery aggravation leakage. Conclusions As cardiac index increased terbutaline we speculate that recruits leaky capillaries increases These findings suggest therapies inducing increase output decrease pulmonary vascular resistances have potential heighten early protein alveoli acutely lung.