Human vascular tissues produce thromboxane as well as prostacyclin.
Human vascular tissues produce thromboxane as well as prostacyclin.
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人体血管组织产生血栓素和前列环素。
DOI：
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发表时间：
1983
影响因子：
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通讯作者：
A. Roberts
中科院分区：
文献类型：
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作者：
J. Mehta;A. Roberts
检查了四种不同类型的人体血管的前列环素 (PGI2) 和血栓素 A2 (TXA2) 的自发释放和花生四烯酸刺激释放情况。自发性PGI2释放量为：脐静脉大于脐动脉，大于隐静脉，大于乳内动脉。通过刺激，所有四种不同血管的 PGI2 释放均显着增加（P 小于 0.001）并且相似。还从所有检查的血管中发现了 TXA2 的自发释放，并且是相似的。随着刺激，TXA2 从所有血管的释放显着增加（P 小于 0.001）。乳内动脉在受到刺激时比其他血管释放更多的 TXA2。 TXA2 的身份通过 TXB2 标准品对 TXB2 抗体的类似置换以及上清液的多次稀释来证实。用阿司匹林治疗血管可抑制 PGI2 和 TXA2 释放，而用 OKY 1581（TXA2 合成酶抑制剂）治疗仅抑制 TXA2 释放。二维薄层色谱显示[14C]花生四烯酸转化为PGI2和TXA2，与放射免疫测定法测量的结果相似。这些数据表明 TXA2 是由人体血管合成的。在较老的血管中，当 PGI2 生成减少时，TXA2 的产生可能具有病理生理学意义。
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.