Lomazova K D, Poliakova A M, Astrina O S, Tsukerman D B
Biull Eksp Biol Med. 1989 May;107(5):538-40.
The effect of PAF in aggregation of platelets induced by endotoxin was studied in experiments in vitro. It is indicated that in high concentration (1.10(-7)-1.10(-6) M) PAF did not affect the degree of aggregation of platelets induced by lipopolysaccharides (LPS) S. typhimurium and N. meningitidis. Successive addition to PRP LPS and PAF or joint addition of PAF and LPS did not change the degree of aggregation of each inductor or their sum. A lower concentration of PAF (1.10(-11)-1.10(-9) M) and endotoxin caused a more expressive aggregation of platelets than their successive addition. Stimulating activity of PAF on endotoxin-induced aggregation, perhaps, is caused by involvement of metabolism of arachidonic acid during blood platelets activation.
在体外实验中研究了血小板活化因子（PAF）对内毒素诱导的血小板聚集的影响。结果表明，高浓度（1×10⁻⁷ - 1×10⁻⁶ M）的PAF不影响鼠伤寒沙门氏菌和脑膜炎奈瑟氏菌脂多糖（LPS）诱导的血小板聚集程度。向富血小板血浆（PRP）中先后加入LPS和PAF或同时加入PAF和LPS，均不会改变每种诱导剂的聚集程度或它们的总和。较低浓度的PAF（1×10⁻¹¹ - 1×10⁻⁹ M）与内毒素共同作用时，比先后加入二者引起的血小板聚集更明显。PAF对内毒素诱导的聚集的刺激活性，可能是由于血小板活化过程中花生四烯酸代谢的参与所致。
