Early reperfusion induces alveolar injury in pulmonary embolism

To observe (1) whether the reperfusion is one of the causes underlying the development of diffuse alveolar injury following pulmonary embolism, and (2) whether polymorphonuclear leukocyte (PMN) accumulation occurs in the reperfused lobe, and (3) whether the production of superoxide is increased from cells obtained by BAL.

The condition of pulmonary embolism was simulated by occluding the pulmonary artery branch using a balloon catheter in anesthetized closed-chest dogs. The occlusion was maintained for 24 h in the occlusion group, and a 2-h period of occlusion was followed by reperfusion in the reperfusion group. Histologic examination was performed at 24 h after occlusion in both groups (n = 8). Using a different group of dogs (n = 12), local cellular changes in the occluded and reperfused lobes were evaluated through BAL performed at 1, 2, and 3 h after reperfusion in the reperfusion group and at 3 h after occlusion in the occlusion group. Superoxide generation from BAL cells was measured by the chemiluminescence method.

There was no histologic evidence of alveolar injury in the occluded lobe, but there were numerous leukocytes and erythrocytes along with exudate and damaged alveoli in the reperfused lobe. In the BAL study, the total cell counts recovered by BAL remained unchanged in all groups. However, the number of PMNs increased significantly in the late stages of reperfusion. Enhanced superoxide generation was observed in BAL cells obtained from reperfused lobe.

Reperfusion is one of the causes underlying the development of alveolar injury in pulmonary embolism by triggering immigration of PMNs to alveoli, which results in the increased superoxide generation in BAL cells.