Stimulation of aggregation and thromboxane A2 formation of human platelets by hypoxia.
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.
D000328:Adult; D000368:Aged; D001792:Blood Platelets / Q000378:metabolism*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000097:blood*; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D010974:Platelet Aggregation; D013928:Thromboxane A2 / Q000097:blood*; D013929:Thromboxane B2 / Q000097:blood; D014652:Vascular Diseases / Q000097:blood
D013929:Thromboxane B2; D013928:Thromboxane A2; D010100:Oxygen