Reperfusion after a two-hour period of pulmonary artery occlusion causes pulmonary necrosis.

The role of reperfusion injury in the progression to necrosis in pulmonary embolism was evaluated. To simulate this condition, we used a technique that enables occlusion and reopening of the pulmonary arterial branch supplying the right upper lobe in conscious rats. The rats were divided into five groups: the occlusion group (n = 12), in which the pulmonary artery (PA) branch was occluded without reperfusion; the reperfusion group (n = 12), in which the PA branch was reopened after a 2-h period of occlusion; and the reperfusion-SOD (n = 9), reperfusion-IM (n = 8), or reperfusion-IA-SOD (n = 6) groups, in which superoxide dismutase (SOD), indomethacin (IM), or inactivated SOD (IA-SOD), respectively, was administered during reperfusion. The lungs were removed 24 h after the PA occlusion, and histologic examination was performed. In the occlusion group, the alveolar structure of the right upper lobe was well preserved, and there was no erythrocyte or leukocyte accumulation. The only significant changes compared with the control lobe was the appearance of wavy internal elastic lamina of the PA and slight neutrophil adherence to the endothelial cells. In contrast, the right upper lobe of the reperfusion group disclosed numerous foci of hemorrhagic necrosis, with disrupted alveoli and leukocyte accumulation in all cases. With SOD treatment, the changes compatible with hemorrhagic necrosis were attenuated to the level of the control lobes. However, neither IM nor IA-SOD decreased these changes.(ABSTRACT TRUNCATED AT 250 WORDS)