Rapid reperfusion causes stress failure in ischemic rat lungs

Objective: Rapid reperfusion may be injurious to the ischemic lung. Our aim was to confirm that slow reperfusion improves postischemic pulmonary funct ion and to elucidate the ultrastructural changes associated with slow versu s rapid reperfusion. Methods: We used an es vivo perfused rat lung transpla nt model to study the effect of slow versus rapid reperfusion on subsequent lung function and morphologic condition. Functional assessment was perform ed in (1) fresh lung, slowly reperfused; (2) fresh lung, rapidly reperfused ; (3) ischemic lung (4 hours at 22 degrees C), slowly reperfused; and (4) i schemic lung, rapidly reperfused. Results: In group 4, the shunt fraction ( P = .001), airway pressure (P = .001), and wet/dry ratio (P = .01) were sig nificantly higher than in groups 1 through 3. Light and electron microscopy of slowly reperfused ischemic lungs (n = 3) appeared normal. Rapidly reper fused ischemic lungs (n = 4) demonstrated massive alveolar edema, hemorrhag e, and epithelial "blebbing" by light microscopy, Electron microscopy ident ified the blebbing as separation of the epithelial layer from an intact bas ement membrane by edema fluid. The epithelial layer was disrupted in numero us locations. Complete disruption of all layers of the blood-gas barrier wa s occasionally present, Conclusion: Rapid reperfusion of the ischemic lung is an important contributing factor to reperfusion lung injury resulting in mechanical stress failure of the alveolar/capillary barrier. Gradual reint roduction of blood flow to the ischemic lung improves oxygenation.