1993 Volume 7 Issue 4 Pages 448-455
Pleural thickening has been reported to be one of late complications after lung transplantation. Although it might be a sequela of operative maneuvers or of the rejection process, the etiology of the pleural changes in lung allografts is still uncertain. To ascertain the cause, pleural changes of lung allografts were investigated histologically and immunohistologically, in a rat lung transplantation model.
The pleura of lung isografts showed no pathological changes except for mild edema on the first day after transplantation. Recipient cells started to migrate into the subpeural tissue of lung allografts early after transplantation (latent phase). In the vascular phase, recipient lymphocytes in the subpleural tissue increased in number. Subsets of the lymphocytes were CD4-positive and CD8-positive cells in almost equal numbers. Macrophages also infiltrated in the area. These infiltrating cells were similar to those in perivascular and peribronchial areas. In the late vascular or alveolar phase, fibroblasts were observed among the infiltrating cells and fibrotic changes started. In the destructive phase, collagen formation with marked pleural thickening was dominant.
In this rat lung transplantation model, the pleura of lung allografts was involved in the rejection process soon after transplantation. Inadequate immunosuppression or repeated rejection could cause pleural changes and lead to functional deterioration of lung allografts because of decreased compliance.
