Prostaglandin production and platelet reactivity of small-diameter grafts

Abstract

This article examines the relationship of platelet deposition to thromboxane and prostacyclin (PGI2) production in arterial autografts (n = 8), para-anastomotic native artery (n = 40), nonseeded control (n = 6), and endothelial cell-seeded (n = 17) small-diameter Dacron grafts implanted in the carotid and femoral arteries of dogs. Platelet deposition was measured by a dual-isotope subtraction platelet-imaging technique that expresses platelet deposition as percent indium excess (%IE). PGI2 and thromboxane assays were performed with the use of an immunoreactive assay. The %IE in the nonseeded grafts was significantly higher than in the seeded prostheses (p < 0.001). Arterial autografts accumulated significantly less platelets than did seeded grafts (p < 0.05) or nonseeded grafts (p < 0.001). The thromboxane A2 (TXA2) production in nonseeded grafts was significantly higher than in seeded grafts (p < 0.001), arterial autografts (p < 0.001), or in para-anastomotic native artery (p < 0.001). The PGI2 production by the arterial autografts was significantly higher than by the nonseeded grafts (p < 0.005), seeded grafts (p < 0.001), or para-anastomotic native artery (p < 0.025). The PGF1α/TXB2 ratio was significantly higher in the arterial autografts when compared with the nonseeded grafts (p < 0.001), endothelial cell-seeded grafts (p < 0.001), or para-anastomotic native artery (p < 0.025). We conclude that platelet deposition can be significantly decreased by endothelial cell seeding of small-diameter grafts. The transmural production of TXA2 by native arteries and prosthetic grafts may have an important influence on platelet deposition and patency. The balance between the production of TXA2 and PGI2 in the graft wall may be the best determinant of platelet deposition and possibly of long-term patency.