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Demonstrates distinct vascular injury patterns driving ischemic pulmonary allograft rejection in modified and unmodified recipients, highlighting vascular damage as a key rejection mechanism.
The morphologic features of pulmonary allograft rejection are described. The graft recipients were either unmodified or treated with Imuran (Azathiaprine), an immunosuppressive agent. The morphological features of graft rejection in the two groups differ, but vascular alterations are a significant feature of both patterns. In unmodified recipients, the earliest changes are the appearance of perivenous mononuclear infiltrates at about 5 days; these progress to involve the vein wall leading to the local disruption of the endothelial and muscular layers. Periarterial mononuclcar infiltrates also appear at about this time, but these initially spare the vessel wall. However, at about 10 days there is progressive mononuclear infiltration of the artery wall as well, primarily subintimal, with concomitant reduction and even obliteration of the arterial lumen. This generalized vasculitis, without vascular necrosis, appears to result in generalized hemorrhagic necrosis of the allograft on an ischemic basis. In the attenuated allograft rejection following immunosuppressive therapy, “chronic” arterial and, to a lesser extent, venous lesions are observed. These show varying degrees of subendothelial inflammation, hyperplasia, and fibrosis. Similar vascular lesions are not found in autografts. The features which distinguish these unique vascular lesions from other forms of allergic vasculitis and the vascular changes found in other types of allografts are described.
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Flax et al. (1966) studied this question.
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