Hirose T, Aoki E, Ishibashi M, Domae M, Ikeda T, Tanaka K
Microvasc Res. 1983 Sep;26(2):193-204. doi: 10.1016/0026-2862(83)90070-5.
Prostacyclin (PG I2) generated by vascular endothelium is a strong antiaggregating substance. As platelet aggregation and release of humoral factor(s) have been reported to be crucial in the pathogenesis of acute lung injury following pulmonary microembolization, PG I2 could have a protective effect against microembolic lung vascular injury. Following unilateral microembolization, we have observed a large increase in the filtration coefficient in the nonembolized lung with a significant increase in 6-keto PG F1 alpha, the stable metabolite of PG I2, in arterial blood. The pretreatment with indomethacin (10 mg/kg) prevented the increase in 6-keto PG F1 alpha and potentiated the lung injury after microembolization. Exogenously administered PG I2 (20 ng/kg/min) prevented completely the increase in the filtration coefficient without any effects on hemodynamics, although these effects of indomethacin and PG I2 did not relate to their effects on platelet aggregation. Based on these results, we could conclude that prostacyclin could play an important role in preserving cell integrity of the lung and in prevention of increased lung vascular permeability following pulmonary microembolization.
血管内皮产生的前列环素（PG I2）是一种强大的抗聚集物质。由于据报道血小板聚集和体液因子释放在肺微栓塞后急性肺损伤的发病机制中起关键作用，PG I2可能对微栓塞性肺血管损伤具有保护作用。单侧微栓塞后，我们观察到未栓塞肺的滤过系数大幅增加，同时动脉血中PG I2的稳定代谢产物6-酮PG F1α显著增加。用吲哚美辛（10 mg/kg）预处理可防止6-酮PG F1α增加，并增强微栓塞后的肺损伤。外源性给予PG I2（20 ng/kg/min）可完全防止滤过系数增加，且对血流动力学无任何影响，尽管吲哚美辛和PG I2的这些作用与其对血小板聚集的作用无关。基于这些结果，我们可以得出结论，前列环素在维持肺细胞完整性以及预防肺微栓塞后肺血管通透性增加方面可能起重要作用。
