内源性高甘油三酯血症患者血浆VLDL、LDL及HDL对血小板聚集功能的影响

目的　研究内源性高甘油三酯血症 (HTG)患者血浆极低密度脂蛋白 (VL DL )、低密度脂蛋白 (L DL )及高密度脂蛋白 (HDL )对血小板聚集功能的影响。方法　对 2 1例内源性高甘油三酯血症患者与 2 1例正常对照者用一次性密度梯度超速离心法分离血浆 VL DL、L DL及 HDL。测定这三种脂蛋白的 2 34nm吸光度 (A2 34 )、电泳迁移率 (REM)及硫代巴比妥酸反应物质 (TBARS)含量。分别将这三种脂蛋白加入由正常人新鲜血浆构成的反应系统中 ,用血小板聚集仪分别测定 ADP诱导的血小板 5 min最大聚集率。结果　内源性 HTG患者血浆 TG含量平均升高 2 .73倍 ,HDL - C下降 1.71倍 ,同时 L PO升高 1.2 2倍 ;HTG组 VL DL、L DL及 HDL的 REM、A2 34 、TBARS含量均较对照组显著增加 (P<0 .0 1) ,表明内源性 HTG患者血浆 VL DL、L DL及 HDL均发生了氧化修饰生成Ox- VL DL、Ox- L DL及 Ox- HDL。血小板聚集率在分别加入 HTG组患者的 VL DL、L DL及 HDL后均比加入正常组相应脂蛋白明显增加 (P<0 .0 5及 P<0 .0 1)。相关分析表明 ,HTG- L DL及 HTG- HDL A2 34 、REM及 TBARS含量与血小板聚集率呈正相关 (P<0 .0 1)。结论　 HTG患者血浆 VL DL、L DL及 HDL发生了氧化修饰 ,并使血小板聚集增加

Effects of Plasma Very Low Density Lipoprotein, Low Density Lipoprotein and High Density Lipoprotein on Platelet Aggregation in Endogenous Hypertrig lyceridemia

Objective To study whether plasma very low density lipoprotein (VLDL), low density lipoprotein (LDL), high density lipoprotein (HDL) were oxidatively modified in endogenous hypertriglyceridemia(HTG) and to investigate the effects of HTG VLDL, LDL and HDL on platelet aggregation in vitro. Methods Blood samples were taken from 21 patients with endogenous triglyceridemia and 21 normal healthy subjects; these two groups were similar in respect to age and sex. Their plasma VLDL, LDL and HDL were isolated by density gradient ultracentrifugation method, and plasma triglycerides (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDLC) were measured by enzyme method. The oxidative modification of LDL, VLDL and HDL was identified by agarose gel relative electrophoretic mobility (REM), absorbance at 234 nm (A 234 ) and fluorescence of thiobarbituric acid reaction substances (TBARS). With the reaction system that consisted of mixed fresh normal plasma, platelet aggregation was induced by adenosine diphosphate(ADP), and the platelet maximal aggregation rate(MAR) was recorded on a 4 channel light aggregometer. Results The plasma TG, TBARS levels in HTG group were 1.6 and 0.4 times over those of the control group respectively ( P< 0.01). The plasma HDLC in HTG group was 32% lower than those of the control group ( P< 0.01). REM, A 234 and TBARS of VLDL, LDL and HDL in HTG group were significantly higher than those in the control group ( P< 0.01). MAR of VLDL, LDL and HDL in HTG group were significantly higher than those in the control group ( P< 0.05). The correlation analysis indicated that REM, A 234 and TBARS of LDL and HDL in HTG group were positively correlated with MAR ( P< 0.01). Conclusion The above data indicated that oxidative modification of plasma VLDL, LDL, HDL did occur in endogenous hypertriglyceridemia in vivo, and VLDL, LDL and HDL enhanced platelet aggregation in vitro.