血管内皮细胞合成前列环素的“捷径”

AN ALTERNATIVE PATHWAY OF PGI: SYNTHESIS BY CULTURED ENDOTHELIAL CELLS FROM PRECURSOR OF TXA: RELEASED FROM ACTIVATED NEUTROPHILS AND PLATELETS

PGI_2和TXA_2是有着共同来源和不同生理活性的物质,参与调节血管紧张性,通透性及血小板聚集。它们分别主要产生于血管内皮细胞和激活的血小板与中性粒细胞。在内皮细胞完整时,内皮细胞可利用由激活血小板及中性粒细胞释放的TXA_2前身物,不经环氧化酶而直接经内皮细胞的PGI_2合成酶产生PGI_2。血管内皮细胞利用这种“捷径”方式,使PGI_2合成量增加,以扩张血管,抑制血小板的聚集,以及对抗TXA_2的作用。

PGI_2 and TXA_2 having common precursors play important roles in the regulation of vasoconstriction, vessel permeability, neutrophil and platelet aggregation and their adherence to blood vessel wall. PGI_2 and TXA_2 are the major products of arachidonic acid metabolites in endothelial cell and activated neutrophil and platelet, respectively.6-keto-PGF_(1α) and TXB_2 were measured in the supernatant of cultured endothelial cells (EC) of various groups. It was found that after the inhibition of cyclooxygenase by indomathecine, EC canstill produce PGI_2 by using precursors released from activated neutrophils and platelets, while the amount of TXA_2 produced by activated neutrophils and platelets in the presence of EC was significantly less than that in the absence of EC.The results indicate that EC can use precursors of TXA_2 released from activated neutrophils and platelets to increase PGI. production and reduca TXB_2 in the culture medium.