Hirose T, Aoki E, Domae M, Ishibashi M, Ikeda T, Tanaka K
Prostaglandins Leukot Med. 1983 May;11(1):51-61. doi: 10.1016/0262-1746(83)90109-9.
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, prostacyclin could have a protective effect against microembolic lung vascular injury. Following unilateral microembolization, the filtration coefficient in the nonembolized lung increased significantly to 0.14 +/- 0.02 from the base line value of 0.07 +/- 0.01 ml/min/mmHg/100g. Prostacyclin as measured as 6-keto PG F1 alpha in arterial blood increased significantly to 4.15 +/- 1.76 at 30 min from the base line value of 1.90 +/- 0.45 ng/ml and increased further to 5.67 +/- 1.49 ng/ml at 60 min following microembolization. Exogenously administered PG I2 methylester (20 ng/kg/min) prevented completely the increase in the filtration coefficient without any effects on hemodynamics, although the effects of PG I2 methylester did not depend on its action on platelet aggregation. Based on these results, we conclude that prostacyclin could play an important role in preserving cell integrity of the lung and prevention of increased lung vascular permeability following pulmonary microembolization.
血管内皮产生的前列环素（PG I2）是一种强效抗聚集物质。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，前列环素可能对微栓塞性肺血管损伤具有保护作用。单侧微栓塞后，未栓塞肺的滤过系数从基线值0.07±0.01 ml/min/mmHg/100g显著增加至0.14±0.02。动脉血中作为6-酮PG F1α测量的前列环素在微栓塞后30分钟时从基线值1.90±0.45 ng/ml显著增加至4.15±1.76，并在60分钟时进一步增加至5.67±1.49 ng/ml。外源性给予前列环素甲酯（20 ng/kg/min）可完全阻止滤过系数的增加，且对血流动力学无任何影响，尽管前列环素甲酯的作用并不依赖于其对血小板聚集的作用。基于这些结果，我们得出结论，前列环素在维持肺细胞完整性和预防肺微栓塞后肺血管通透性增加方面可能起重要作用。
