Ultrastructural alterations in intraalveolar surfactant subtypes after experimental ischemia and reperfusion

Ischemia and reperfusion (I/R) result in surfactant dysfunction. Whether th e impairment of surfactant is a consequence or a cause of intraalveolar ede ma formation is still unknown. The cumulative effects of lung perfusion, is chemic storage, and subsequent reperfusion on surfactant ultrastructure and pulmonary function were studied in a rat isolated perfused lung model. The left lungs were fixed for electron microscopy by vascular perfusion either immediately after excision (control; n = 5) or after perfusion with modifi ed Euro-Collins solution (EC), storage for 2 h at 4 degrees C in EC, and re perfusion for 40 min (n = 5). A stereological approach was chosen to discri minate between intraalveolar surfactant subtypes of edematous regions and r egions free of edema. Intraalveolar edema seen after I/R in the EC group oc cupied 36 +/- 6% (mean +/- SEM) of the gas exchange region as compared with control lungs (1 +/- 1%; p = 0.008). Relative intraalveolar surfactant com position showed a decrease in surface active tubular myelin (3 +/- 1 versus 12 +/- 0%; p = 0.008) and an increase in inactive unilamellar forms (83 +/ - 2 versus 64 +/- 5%; p = 0.008) in the EC group. These changes occurred bo th in edematous (tubular myelin, 3 +/- 1%; unilamellar forms, 88 +/- 6%) an d in nonedematous regions (tubular myelin, 4 +/- 3%; unilamellar forms, 77 +/- 5%). The ultrastructural changes in surfactant were associated with an increase in peak inspiratory pressure during reperfusion. In conclusion, su rfactant alterations seen after I/R are not directly related to the presenc e of edema fluid in the alveoli. Disturbances in intraalveolar surfactant a fter I/R are not merely the result of inactivation due to plasma protein le akage but may instead be responsible for an increased permeability of the b lood-air barrier, resulting in a vicious cycle of intraalveolar edema forma tion and progressing surfactant impairment.