Pirich C, Banyai M, Efthimiou Y, Sinzinger H
Wilhelm Auerswald Atherosclerosis Research Group (ASF) Vienna, Austria.
Semin Thromb Hemost. 1993;19(2):138-43. doi: 10.1055/s-2007-994017.
PGI2 is an important local mediator keeping circulating blood cells apart from the vessel wall, thus regulating hemostasis. Alterations of locally available amounts of this compound may be associated with either bleeding or thrombotic events. Factors influencing synthesis, transmission, and degradation coregulate the amount of biologically active PGI2 available at a certain vascular site. Plasmatic T1/2 of PGI2 is shortened either due to an inherited disorder or an acquired disease, its underlying cause being unknown. Generally, this is associated with thrombotic events and extremely low concentrations of both HDL cholesterol and apoA1. In contrast, the only patient we saw with a prolonged PGI2 T1/2 repeatedly experienced extremely severe bleeding complications. Recovery from severe diseases such as shock and malaria, for example, results in normalization of both PGI2 T1/2 and lipoprotein (HDL) and apoA values. Although these findings have not yet been verified at a molecular level, it is likely, that apoA1 contributes to the stabilization of PGI2 in human blood, thus representing one further link between lipid metabolism and hemostasis.
前列环素（PGI2）是一种重要的局部介质，可使循环血细胞与血管壁分离，从而调节止血。该化合物局部可用量的改变可能与出血或血栓形成事件相关。影响合成、传递和降解的因素共同调节特定血管部位生物活性PGI2的可用量。PGI2的血浆半衰期缩短，原因可能是遗传性疾病或后天性疾病，但其根本原因尚不清楚。一般来说，这与血栓形成事件以及高密度脂蛋白胆固醇（HDL胆固醇）和载脂蛋白A1（apoA1）的极低浓度有关。相反，我们所见到的唯一一位PGI2半衰期延长的患者反复出现极其严重的出血并发症。例如，从休克和疟疾等严重疾病中恢复后，PGI2半衰期以及脂蛋白（HDL）和载脂蛋白的值均恢复正常。尽管这些发现尚未在分子水平上得到证实，但载脂蛋白A1可能有助于PGI2在人体血液中的稳定，因此代表了脂质代谢与止血之间的另一个联系。
