Human vascular tissues produce thromboxane as well as prostacyclin.

Four different types of human blood vessels were examined for spontaneous and arachidonate-stimulated release of prostacyclin (PGI2) and thromboxane A2 (TXA2). Spontaneous PGI2 release was umbilical veins greater than umbilical arteries greater than saphenous veins greater than internal mammary arteries. With stimulation, PGI2 release by all four different vessels increased significantly (P less than 0.001) and was similar. Spontaneous release of TXA2 was also identified from all vessels examined and was similar. With stimulation, TXA2 release from all vessels increased significantly (P less than 0.001). Internal mammary artery released more TXA2 than other vessels on stimulation. The identity of TXA2 was confirmed by similar displacement of TXB2 antibody by TXB2 standards and by multiple dilutions of supernates. Treatment of vessels with aspirin inhibited PGI2 as well as TXA2 release, whereas treatment with OKY 1581 (TXA2 synthetase inhibitor) inhibited TXA2 release only. Two-dimensional thin-layer chromatography showed [14C]arachidonate conversion to PGI2 and TXA2 similar to that measured by radioimmunoassay. These data suggest that TXA2 is synthesized by human vessels. In older vessels when PGI2 generation is decreased, TXA2 production may by of pathophysiological significance.