Pönicke K, Sternitzky R, Mest H J
Department of Pharmacology and Toxicology, Martin Luther University, Halle, GDR.
Prostaglandins Leukot Med. 1987 Sep;29(1):49-59. doi: 10.1016/0262-1746(87)90096-5.
The influence of hypoxia on the spontaneous platelet aggregation (SPA) and thromboxane formation was studied. The analysis of aggregation curve was carried out according to Breddin. The hypoxia enhanced the aggregability from Q2norm = 2.46 +/- 0.40 (normoxia) to Q2hyp = 4.39 +/- 0.39 (hypoxia), n = 52, p less than 0.001. 10 samples of those showed no SPA under equilibration with air but the hypoxic stimulus provoked SPA (Q2norm = 0, Q2hyp = 1.19 +/- 60, n = 10, p less than 0.001). When the results were arranged according to the degree of the stimulation of SPA, two groups could be separated with low and high response to hypoxia. The hypoxia caused also an augmentation of the TXB2 level in comparison to normoxia. The stronger enhancement of the TXB2 formation during the incubation under hypoxic conditions was independent of the fact whether SPA took place or not. The present study suggests that hypoxic conditions alone may be a reason for a stimulated TXA2 formation of the platelets and that the enhanced TXA2 formation caused by hypoxia is possibly inducing or reinforcing the SPA.
研究了缺氧对血小板自发聚集（SPA）和血栓素形成的影响。根据布雷丁方法对聚集曲线进行分析。缺氧使聚集性从正常氧合时的Q2norm = 2.46±0.40增强至缺氧时的Q2hyp = 4.39±0.39，n = 52，p < 0.001。其中10个样本在与空气平衡时未出现SPA，但缺氧刺激引发了SPA（Q2norm = 0，Q2hyp = 1.19±60，n = 10，p < 0.001）。当根据SPA刺激程度整理结果时，可分为对缺氧反应低和高的两组。与正常氧合相比，缺氧还导致TXB2水平升高。在缺氧条件下孵育期间TXB2形成的更强增强与SPA是否发生无关。本研究表明，单纯缺氧条件可能是血小板TXA2形成受刺激的原因，且缺氧导致的TXA2形成增强可能诱导或加强了SPA。
