Transplant arterial vasculopathy: evidence for a dual pattern of endothelial injury and the source of smooth muscle cells in lesions of intimal hyperplasia.

With use of this straight artery model of transplantation for studying TGVD, we have shown the following: 1. Intimal thickening occurs in a time-dependent predictable manner only in allografts. 2. Endothelial injury as a result of procurement, preservation, and reperfusion by itself does not result in the development of intimal thickening. Additional endothelial injury associated with the presence of an early mononuclear infiltrate is necessary for the development of TGVD. 3. The development of intimal hyperplasia is initially cellular, consisting mainly of macrophages and a smaller proportion of lymphocytes. The macrophages are later replaced by SMCs. These findings are summarized in Figure 16. 4. The source of the SMCs in intimal lesions is most likely the recipient media.