OBJECTIVE: To examine the changes in brush cytology during acute small bowel allograft rejection and to evaluate the usefulness of cytology in detecting acute rejection. STUDY DESIGN: Heterotopic porcine small bowel allografts were followed by brush cytology and full-thickness biopsies during unmodified rejection. RESULTS: The most prominent changes in cell differential counts were an increase in the proportion of granulocytes and decrease in the proportion of epithelial cells. In brushed epithelial fragments, infiltration of granulocytes and acidophilia increased, and cell cohesion was gradually lost with the degeneration of nuclei and necrosis of epithelium. The cell differential count was compared to the histologic acute rejection index, which was created on the basis of five semiquantitatively evaluated histologic parameters. The sensitivity of cell differentiation in detecting histologically moderate or severe rejection was 87% (13 of 15 cases) and the specificity 76% (5 false positives in 21 negative cases). CONCLUSION: Suspicion of acute rejection can be assessed with reasonable reliability by cytology, but it cannot be detected earlier than by histology. Brush cytology complements mucosal biopsies in the evaluation of rejection and, as a rapid and cost-effective method, may even partly replace them. It may also prove valuable in detecting opportunistic bowel infections in immunosuppressed patients.

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Chronic rejection in rat aortic allografts. An experimental model for transplant arteriosclerosis.

Chronic rejection has several histological appearances, depending on the type of organ graft. Common to all of them is transplant arteriosclerosis associated with an ongoing inflammatory response in the transplanted graft. To the contrary of classical atherosclerosis, in which the manifestations are mostly focal, proximal, and asymmetric, transplant arteriosclerosis is generalized, and the intimal thickening is concentric. In this article, we describe an experimental animal model whereby transplant arteriosclerosis may be investigated in the inbred rat. Aortic allografts were transplanted from DA (RTIa) to major histocompatibility complex-incompatible WF (RTIv) rats or, for control, to rats of the DA strain. Transplantation was followed by an acute inflammation episode in the aortic adventitia of the allograft, largely lacking in the syngeneic graft, with a prominence of lymphoid activation markers (Cd25) in the cells of the inflammatory infiltrate. The inflammation episode peaked at 2 months after transplantation, became attenuated, and was followed by a proliferative response of myocytes in the allograft media. An increase in the migration of myocytes to the subendothelial space (presumably through small breaks generated in the internal elastic lamina) was observed thereafter, and myocyte proliferation continued in the intima with some intermingled macrophages. Finally, necrosis and disappearance of myocytes and their replacement by fibrous tissue were observed in the media. These alterations are virtually identical with the vascular lesion of chronically rejecting parenchymal organ transplants in human subjects. We suggest that aortic allografts exchanged between histoincompatible rat strains may be used as an experimental model for transplant arteriosclerosis.

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