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目的：观察冠状动脉（冠脉）发生周期性血流减少（ＣＦＲｓ）时血栓烷Ａ２（ＴＸＡ２）及前列环素（ＰＧＩ２）的变化及意义。方法：犬剖胸分离出２～３ｃｍ长的冠脉前降支（ＬＡＤ），用血管钳钳夹方法损伤冠脉内膜后放置血管缩窄环，使冠脉达临界狭窄。缩窄环近端置电磁流量计，诱发ＣＦＲｓ，在ＣＦＲｓ出现前及ＣＦＲｓ出现后４０ｍｉｎ冠状窦内采血，用放免法测ＴＸＡ２及ＰＧＩ２的代谢产物ＴＸＢ２及６－Ｋ－ＰＧＦ１α。结果：ＣＦＲｓ出现４０ｍｉｎ后，ＴＸＢ２及６－Ｋ－ＰＧＦ１α均显著升高（Ｐ＜０．０１）（ＴＸＢ２从７５．６２±４８．８７ｎｇ／Ｌ升至１０９．２２±４５．９９ｎｇ／Ｌ；６－Ｋ－ＰＧＦ１α从１６．１４±９．２８ｎｇ／Ｌ升至３５．５７±１７．２１ｎｇ／Ｌ）。结论：发生ＣＦＲｓ时，血管内皮细胞分泌的６－Ｋ－ＰＧＦ１α随血小板分泌的ＴＸＢ２一同显著升高，其机理可能是血管内皮细胞的一种应激性反应。
Objective: To observe the changes and significance of thromboxane A2 (TXA2) and prostacyclin (PGI2) in patients with coronary artery (coronary artery) with periodic blood flow reduction (CFRs). Methods: The anterior descending coronary artery (LAD) of 2 ~ 3 cm in length was isolated from the thoracotomy of the dog. The vasoconstriction ring was placed after the intima of the coronary artery was injured by vasoconstrictor and the critical coronary artery was stenosed. The CFRs were induced by narrowing the proximal electromagnetic flowmeter. Blood samples were taken from the coronary sinus 40 min before and after the appearance of CFRs. The TXB2 and 6-K-PGF1α metabolites of TXA2 and PGI2 were detected by radioimmunoassay. Results: TXB2 and 6-K-PGF1α were significantly increased after 40min CFRs (P <0.01), TXB2 increased from 75.62 ± 48.87ng / L to 109.22 ± 45.99ng / L; -K-PGF1α increased from 16.14 ± 9.28 ng / L to 35.57 ± 17.21 ng / L). CONCLUSIONS: In the presence of CFRs, 6-K-PGF1α secreted by vascular endothelial cells significantly increases with TXB2 secreted by platelets, which may be a stress response of vascular endothelial cells.