Bjøro K
Prostaglandins. 1986 Apr;31(4):699-714. doi: 10.1016/0090-6980(86)90175-9.
The formation of prostacyclin (PGI2) and thromboxane A2 (TXA2) (measured as the stable metabolites 6-keto-PGF1 alpha and TXB2) during stimulation with vasoactive autacoids was registered in human umbilical arteries perfused in vitro. Responses were registered within 3-4 minutes after addition of the substances. Both angiotensin I and II were found to increase the formation of PGI2 while depressing that of TXA2. Serotonin increased the formation of TXA2 but not that of PGI2. Both PGE2 and PGF2 alpha stimulated the PGI2 formation. The TXA2 mimetic U46619, increased PGI2 production, whereas PGI2 slightly increased the formation of TXA2. All responses were found to be completely inhibited by indomethacin.
在体外灌注的人脐动脉中，记录了血管活性自分泌物质刺激过程中前列环素（PGI2）和血栓素A2（TXA2）（以稳定代谢产物6-酮-PGF1α和TXB2衡量）的生成情况。在添加物质后3 - 4分钟内记录反应。发现血管紧张素I和II均能增加PGI2的生成，同时抑制TXA2的生成。5-羟色胺增加TXA2的生成，但不增加PGI2的生成。PGE2和PGF2α均刺激PGI2的生成。TXA2模拟物U46619增加PGI2的产生，而PGI2则轻微增加TXA2的生成。发现所有反应均被吲哚美辛完全抑制。
