Luminal release of prostacyclin and thromboxane A2 by arteries distal to small-caliber prosthetic grafts.

Myointimal hyperplasia distal to prosthetic grafts may be due to a local imbalance of prostacyclin and thromboxane A2 that exaggerates platelet adherence. This study evaluated prostacyclin and thromboxane A2 production by arteries distal to prosthetic grafts. In 12 dogs, control segments of both iliac arteries were excised and a 5 cm segment of polytetrafluoroethylene was grafted end to end. One iliac artery was circumferentially dissected from the distal anastomosis to the inguinal ligament. The contralateral artery was not dissected. Of the 24 grafts, 19 remained patent and the arteries distal to these grafts were studied. After excision, each artery was analyzed for its ability to produce prostacyclin and thromboxane A2. Our data indicate that the luminal surface of a normal artery spontaneously produces both prostacyclin and thromboxane A2 and that the arterial wall distal to a prosthetic graft produces increased levels of these arachidonic acid metabolites. However, only those arteries not surgically dissected maintain a normal balance of prostacyclin and thromboxane A2. The dissected artery may thus be more susceptible to platelet interaction and myointimal hyperplasia.