The effect of bromocryptine-induced hypoprolactinemia on xenogeneic and allogeneic skin graft survival in a mouse model.

Bromocryptine-induced hypoprolactinemia produces immunosuppression capable of extending allograft survival in solid organ transplantation models, but its potential for delaying either xenogeneic or allogeneic skin graft rejection is as yet undefined. In this study the ability of bromocryptine to prolong the survival of either cutaneous human xenografts or murine allografts was compared with cyclosporin A in a mouse model. In xenograft experiments cryopreserved human cadaver skin was grafted to B6D2F1 mice. In allograft experiments skin graft donors (A/J mice) differed genetically from recipients (Balb-C mice) at the major histocompatibility locus. In the untreated control group xenograft survival averaged 7 days and allograft survival 8 days. Xenograft rejection was delayed significantly and nearly equally by both bromocryptine and cyclosporin A (mean 15 and 16 days, respectively). However, allograft rejection was delayed longer by cyclosporin A (mean 24 days; p = 0.0002) than by bromocryptine (mean 15 days; p = 0.066). Administration of porcine prolactin (1 mg) partially reversed the bromocryptine effect (mean xenograft survival, 11 days; mean allograft survival, 10 days). The results of this study suggest that the immunosuppression of prolactin release by bromocryptine may be an effective, benign means of prolonging the survival of biologic dressings (e.g., banked cadaver allograft or porcine xenograft) used for temporary wound coverage in massively burned patients.