The success of transplantation has resulted in increasing demand, despite a
continuing fall, in donor organ supply. This widening gap encourages the a
rgument for animals to act as a reservoir for donor organs (xenografts). De
spite genetic manipulation, transgenic xenograft organs are at risk of vasc
ular rejection in man (delayed xenograft rejection), a process in part invo
lving endothelial cell activation. It appears that ischemia-reperfusion inj
ury also involves endothelial cell activation. Evidence already exists to s
upport the suggestion that ischemia-reperfusion injury may promote delayed
xenograft rejection. The mechanisms of both these processes are briefly des
cribed and a case is made for optimum organ preservation of transgenic xeno
graft donor organs before clinical work is proposed.