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Widespread platelet aggregation and microvascular endothelial damage are characteristic features of the early post transplant phase of hyperacute rat cardiac allograft rejection. Vascular staining for rat C3 and rat IgG are consistent immunohistochemical correlates of these alterations. In order to determine the role of platelets and of complement in the pathogenesis of microvascular destruction in hyperacute rejection, a series of ACI rat cardiac allografts and LEWIS (LEW) syngeneic heart grafts transplanted to ACI skin presensitized LEW recipients were studied over the initial 15 minutes posttransplantation. Intravenously administered colloidal carbon was utilized as a tracer for detection of vascular damage by combined light and electron microscopy. All allografts in unmodified combinations showed extensive platelet aggregation and microvascular endothelial damage. Allografts transplanted to recipients in which C3 had been effectively depleted by cobra venom factor showed no microvascular alterations and were comparable to syngeneic controls. There was no depression of recipient platelet counts in the C3 depleted group at the time of transplantation. Allografts transplanted to recipients in which a profound thrombocytopenia had been induced as a result of prior administration of a rabbit antirat platelet globulin preparation showed extensive microvascular destruction at 15 minutes posttransplantation. Recipient platelet depleted syngeneic heart grafts showed no vascular alterations and were comparable to unmodified syngeneic controls. There was no depression of serum hemolytic C3 in platelet depleted recipients at the time of heart graft placement. This study indicates that complement activated by donor specific alloantibodies may directly induce endothelial damage in hyperacute rat cardiac allograft rejection and that platelets are not critical initiators of this process.

Controlled Studies On The Pathogenesis Of Microvascular Endothelial Damage In Hyperacute Cardiac Allograft Rejection