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1 Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, United States
2 Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, United States; CVRI, UCSF, San Francisco, California, United States
3 Anesthesiology, UCSF Medical Center, San Francisco, California, United States
4 Keio University; Keio University, United States
5 Anesthesiology, Tokyo Medical and Dental University, Tokyo, Japan
6 University of California, San Francisco, Cardiovascular Reseach Institute, San Francisco, California, United States
* To whom correspondence should be addressed. E-mail: frankja{at}itsa.ucsf.edu.
To study airspace fluid clearance (AFC) under conditions that resemble the clinical setting of pulmonary edema in patients, we developed a new perfused human lung preparation. We measured AFC in 20 human lungs rejected for transplantation and determined the contribution of AFC to lung fluid balance. AFC was then compared with airspace and perfusate levels of a biological marker of epithelial injury. The majority of human lungs rejected for transplant had intact basal (75%) and 
2-adrenergic agonist-stimulated (70%) AFC. For lungs with both basal and stimulated AFC, the basal AFC rate was 19 ± 10%/h and the β2-adrenergic-stimulated AFC rate was 43 ± 13%/h. Higher rates of AFC were associated with less lung weight gain (Pearson coefficient -0.90, P<0.0001). Airspace and perfusate levels of the type I pneumocyte marker RAGE were 3-fold and 6-fold higher respectively in lungs without basal AFC compared with lungs with AFC (P<0.05). These data show that preserved AFC is a critical determinant of favorable lung fluid balance in the perfused human lung, raising the possibility that 2-agonist therapy to increase edema fluid clearance may be of value for patients with acute lung injury and pulmonary edema. Also, although additional studies are needed, a biological marker of alveolar epithelial injury may be useful clinically in predicting preserved AFC.
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