EARLY REPERFUSION INDUCES ALVEOLAR INJURY IN PULMONARY-EMBOLISM

Study objective: 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 produ ction of superoxide is increased from cells obtained by BAL. Design: T he condition of pulmonary embolism was simulated by occluding the pulm onary artery branch using a balloon catheter in anesthetized closed-ch est 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 rep erfusion group. Histologic examination was performed at 24 h after occ lusion in both groups (n=8). Using a different group of dogs (n=12), l ocal cellular changes in the occluded and reperfused lobes were evalua ted through BAL performed at 1, 2, and 3 h after reperfusion in the re perfusion group and at 3 h after occlusion in the occlusion group. Sup eroxide generation from BAT, cells was measured by the chemiluminescen ce method. Results: There was no histologic evidence of alveolar injur y in the occluded lobe, but there were numerous leukocytes and erythro cytes along with exudate and damaged alveoli in the reperfused lobe. I n the BAL study, the total cell counts recovered by BAL remained uncha nged in all groups. However, the number of PMNs increased significantl y in the late stages of reperfusion. Enhanced superoxide generation wa s observed in BAL cells obtained from reperfused lobe. Conclusion: Rep erfusion is one of the causes underlying the development of alveolar i njury in pulmonary embolism by triggering immigration of PMNs to alveo li, which results in the increased superoxide generation in BAL cells.