Hyperacute rejection of cardiac allografts in a rat strain with a hereditary platelet function defect

Graft hypoperfusion secondary to widespread vascular occlusion by recipient-derived platelet aggregates may be a major determinant of hyperacute cardiac allograft rejection in the rat. Since a hereditary platelet aggregation defect, attributed to decreased platelet levels of serotonin and adenine nucleotides and a depressed release reaction, has been described in the fawn-hooded rat strain, the effects of this intrinsic platelet function defect on the time course and morphologic features of hyperacute rejection have been evaluated. A series of nine heterotopic ACI cardiac allografts in fawn-hooded recipients actively immunized with ACI skin grafts were studied. Functional rejection with asystole was observed in all allografts from 8 to 40 minutes posttransplantation. Widespread platelet aggregation, endothelial cell destruction, interstitial widening, and focal myocardial alterations consistent with ischemic damage characterized all allograft. This study indicates that the platelet aggregation defect described for the fawn-hooded rat strain is one that does not alter the time course of the morphologic features of hyperacute cardiac allograft rejection, and thus this platelet aggregation abnormality has no essential role in the pathogenesis of this type of tissue damage.