Polymorphonuclear leukocytes are activated during atelectasis before lung reexpansion in rat.

Although reexpansion of a collapsed lung often causes pulmonary edema, the pathogenesis of the condition is not yet fully understood. To determine whether inflammatory changes occur in the pulmonary circulation during atelectasis and study the mechanism underlying the development of reexpansion pulmonary edema, we used a rat model in which the left lung was collapsed by bronchial occlusion for 1 h and then reexpanded and ventilated for an additional 1 h. We evaluated the accumulation of polymorphonuclear leukocytes (PMNs) in the lung and the production of reactive oxygen species (ROS) in the pulmonary circulation using a fluorescent imaging technique. We also used confocal laser scanning microscopy and computerized image analysis to evaluate the membrane translocation of p47-phox, one of the nicotinamide adenine dinucleotide phosphate (reduced form) oxidase subunits, in PMNs sequestered in the lung. Polymorphonuclear leukocytes accumulated in the lung during atelectasis, and p47-phox was translocated to the plasma membrane, but no ROS production was observed. Marked PMN ROS production was observed after reexpansion of the collapsed lung with air. Little ROS production was observed when the lung was reexpanded with nitrogen. During atelectasis, PMNs accumulate in the lung, where they are primed for respiratory bursting. After pulmonary reexpansion, oxygen is supplied from the alveoli, and PMN respiratory bursting occurs.