Preservation, reperfusion, and rejection in transgenic xenograft organs.
The success of transplantation has resulted in increasing demand, despite a continuing fall, in donor organ supply. This widening gap encourages the argument for animals to act as a reservoir for donor organs (xenografts). Despite genetic manipulation, transgenic xenograft organs are at risk of vascular rejection in man (delayed xenograft rejection), a process in part involving endothelial cell activation. It appears that ischemia-reperfusion injury also involves endothelial cell activation. Evidence already exists to support the suggestion that ischemia-reperfusion injury may promote delayed xenograft rejection. The mechanisms of both these processes are briefly described and a case is made for optimum organ preservation of transgenic xenograft donor organs before clinical work is proposed.
Goddard
M
M
Department of Pathology, Papworth Hospital, Papworth Everard, England.
Large
S R
SR
D000818:Animals; D004730:Endothelium, Vascular / Q000502:physiology*; D006084:Graft Rejection / Q000503:physiopathology* / Q000517:prevention & control; D006801:Humans; D015427:Reperfusion Injury / Q000503:physiopathology* / Q000517:prevention & control; D014183:Transplantation, Heterologous