SummaryVascular prostacyclin (PGI2) production is different in the arteries and veins of the dog. Experiments were performed to determine whether chronic grafting of the femoral vein into the arterial circulation would alter the normal PGI2 and thromboxane (TxA2) synthesis of the “arterialized” veins. Spontaneous and arachidonic acid (AA) stimulated PGI2 and TxA2 production (measured by radioimmunoassay of 6-keto PGF1α and TxB2 respectively) were analysed in full thickness punch biopsies of the middle part of the grafts after 3 and 16 months and compared with unoperated veins and arteries. PGI2 production was significantly higher in arteries than in veins but no significant difference in TxB2 production was found. Middle “arterialized” venous graft produced significantly lower amounts of PGI2 and higher amounts of TxB2 than unoperated vessels. PGI2 production was more reduced in the distal than in the middle or the proximal parts of the venous grafts especially when stimulated with AA. These findings do not support the concept that the venous graft was biochemically adapted or “arterialized” in terms of PGI2 production when implanted for 3 months or longer. Rather the markedly decreased PGI2/TxB2 ratio in the middle of the graft may be a contributory cause of thrombogenicity and may be implicated in the pathogenesis of neointimal hyperplasia.

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