INHIBITION OF PLATELET INTEGRIN GPIIbIIIa PROLONGS SURVIVAL OF DISCORDANT CARDIAC XENOGRAFTS1, 2

D Candinas, BA Lesnikoski, WW Hancock, I Otsu… - …, 1996 - journals.lww.com
D Candinas, BA Lesnikoski, WW Hancock, I Otsu, N Koyamada, AP Dalmasso, SC Robson
Transplantation, 1996journals.lww.com
The integrin GPIIbIIIa is known to be crucial to the formation of platelet aggregates and
potentiates adhesion to subendothelial matrices via fibrin (ogen), von Willebrand factor, and
vitronectin. Given the demonstration by us and others of widespread platelet aggregation
during xenograft rejection, we hypothesized that platelet thrombi might contribute to graft
dysfunction during development of hyperacute rejection (HAR), as well as during what we
have termed delayed xenograft rejection (DXR), eg, as seen in complement-depleted rat …
Abstract
The integrin GPIIbIIIa is known to be crucial to the formation of platelet aggregates and potentiates adhesion to subendothelial matrices via fibrin (ogen), von Willebrand factor, and vitronectin. Given the demonstration by us and others of widespread platelet aggregation during xenograft rejection, we hypothesized that platelet thrombi might contribute to graft dysfunction during development of hyperacute rejection (HAR), as well as during what we have termed delayed xenograft rejection (DXR), eg, as seen in complement-depleted rat recipients of guinea pig cardiac xenografts. We therefore tested the effects of a specific GPIIbIIIa antagonist (SDZ GPI 562) during xenograft rejection.
Lippincott Williams & Wilkins