血液透析期间血浆中6-氧代前列环素F1α水平升高。

Enhanced 6-oxo-PGF1 alpha levels in plasma during hemodialysis.

作者信息

Leithner C, Sinzinger H, Stummvoll H K, Klein K, Silberbauer K, Peskar B A

出版信息

Prostaglandins Med. 1980 Dec;5(6):425-7. doi: 10.1016/0161-4630(80)90066-x.

Abstract

The activation of platelets due to foreign surface interaction is a well known fact. Earlier, we found an increase of circulating platelet microaggregates (method of Wu and Hoak) during hemodialysis. Since this phenomenon might cause a PGI2-release by lung and/or vascular tissue, we studied the plasma 6-oxo-PGF 1 alpha-levels in 6 patients during hemodialysis. We found an initial increase of plasma 6-oxo-PGF 1 alpha. Coincidently, hypoxemia, fall in platelet and lekocyte count and a decrease in platelet count ratio were observed. An effect of heparin was excluded in a control group. The findings support the hypothesis that PGI2 acts as a defense mechanism against platelet deposition on vascular wall by a temporary increased synthesis which could be monitored by a temporarily enhanced plasma 6-oxo-PGF 1 alpha-level during the initial phase of hemodialysis.

摘要

由于异物表面相互作用导致血小板活化是一个众所周知的事实。此前，我们发现血液透析期间循环血小板微聚体（Wu和Hoak方法）有所增加。鉴于这种现象可能会导致肺和/或血管组织释放前列环素（PGI2），我们研究了6例患者在血液透析期间的血浆6-氧代-PGF1α水平。我们发现血浆6-氧代-PGF1α最初有所增加。同时，观察到低氧血症、血小板和白细胞计数下降以及血小板计数比例降低。在一个对照组中排除了肝素的影响。这些发现支持了这样的假设，即PGI2通过暂时增加合成来充当一种防御机制，防止血小板沉积在血管壁上，这可以通过血液透析初始阶段血浆6-氧代-PGF1α水平的暂时升高来监测。