Hirudin reduces tissue factor expression and attenuates graft arteriosclerosis in rat cardiac allografts

BACKGROUND-Intravascular clotting has been implicated in the pathogenesis of cardiac allograft vasculopathy (CAV). We previously identified the expression of tissue factor (TF), the primary cellular initiator of blood coagulation, within the coronary intima, which was associated with neointimal thic...

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Veröffentlicht in:Circulation (New York, N.Y.) N.Y.), 2000-07, Vol.102 (3), p.357-363
Hauptverfasser: HÖLSCHERMANN, H, BOHLE, R. M, SCHMIDT, H, ZELLER, H, FINK, L, STAHL, U, GRIMM, H, TILLMANNS, H, HABERBOSCH, W
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Sprache:eng
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Zusammenfassung:BACKGROUND-Intravascular clotting has been implicated in the pathogenesis of cardiac allograft vasculopathy (CAV). We previously identified the expression of tissue factor (TF), the primary cellular initiator of blood coagulation, within the coronary intima, which was associated with neointimal thickening. In the present study, the effect of recombinant hirudin on CAV was assessed in Lewis to Fisher rat heterotopic cardiac allografts. METHODS AND RESULTS-Transplant recipients were randomized to a control group (n=10) and a hirudin-treated group (n=12; 2 mg. kg(-1). d(-1) SC). Histological evaluations of rejection, CAV, and TF staining were performed 120 days after transplantation. No significant differences were observed between the 2 groups with respect to the degree of rejection. Hirudin significantly (P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.102.3.357