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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 are substances with common sources and different physiological activities involved in the regulation of vascular tone, permeability and platelet aggregation. They are mainly produced in vascular endothelial cells and activated platelets and neutrophils, respectively. Endothelial cells, when endothelial cells are intact, utilize the precursor of TXA2 released by activated platelets and neutrophils, producing PGI2 directly via the endothelial cell’s PGI2 synthase without cyclooxygenase. Vascular endothelial cells take advantage of this “shortcut” approach to increase PGI2 synthesis to dilate blood vessels, inhibit platelet aggregation, and counteract the effects of TXA_2.