Prostaglandin production and platelet reactivity of small-diameter grafts

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 PGF_1α/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.