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首页> 外文期刊>Life sciences >Effect of low doses of ethanol on platelet function in long-life abstainers and moderate-wine drinkers.
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Effect of low doses of ethanol on platelet function in long-life abstainers and moderate-wine drinkers.

机译：低剂量乙醇对长寿命戒酒者和中酒饮用者的血小板功能的影响。

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摘要

In vitro, high concentrations of ethanol (EtOH) reduce platelet aggregation. Less is known about the effect of low EtOH doses on platelet function in a selected human population of long-life abstainers and low moderate-wine drinkers to avoid rebound effect of EtOH on platelet aggregation. Results of our experiments suggest that moderate-wine drinkers have higher levels of high density lipoprotein (HDL) than long-life abstainers while fibrinogen levels are unchanged. Furthermore, platelets obtained from these individuals do not differ in their response when stimulated by agonists such as AA and collagen. The effect of in vitro exposure of low doses of EtOH has been studied in PRP and in washed platelets. EtOH (0.1-10 mM) inhibits platelet aggregation induced by collagen at its ED50 while is ineffective when aggregation was triggered by U-46619 and by 1 microM adenosine diphosphate (ADP). 5-10 mM EtOH partially reduces the second wave of aggregation induced by 3 microM ADP. 0.1-10 mM EtOH dose-dependently lowers the aggregation induced by AA at its ED50 but it is less effective at ED75 of AA. The antiaggregating effect of EtOH on aggregation induced by AA is unchanged by inhibitor of nitric oxide synthase. In addition, 10 mM EtOH reduces thromboxane (Tx) formation. In washed platelets, 1-10 mM EtOH partially inhibits platelet aggregation induced by thrombin. In washed resting platelets, 10 mM EtOH does not change the resting [Ca++]i while significantly reduces the increase in [Ca++]i triggered by AA. The results of ex vivo experiments have demonstrated that wine increases the HDL. However, this observation may or may not influence the response of platelets to agonists. Results of our studies demonstrate that low doses of alcohol reduces platelet function.
机译：在体外，高浓度乙醇（EtOH）会降低血小板聚集。对于选择的长寿命戒酒者和低度中酒饮用者人群，低剂量的EtOH对血小板功能的影响知之甚少，以避免EtOH对血小板聚集的反弹作用。我们的实验结果表明，中酒饮用者的高密度脂蛋白（HDL）水平高于长寿者，而纤维蛋白原水平却没有变化。此外，从这些个体获得的血小板在被诸如AA和胶原的激动剂刺激时，其反应没有差异。在PRP和洗涤过的血小板中已研究了低剂量EtOH的体外暴露效果。 EtOH（0.1-10 mM）在其ED50时抑制胶原蛋白诱导的血小板凝集，而在由U-46619和1 microM腺苷二磷酸（ADP）触发凝集时无效。 5-10 mM EtOH部分减少了3 microM ADP诱导的第二次聚集波。 0.1-10 mM EtOH剂量依赖性地降低AA在其ED50时诱导的聚集，但在AA的ED75时效果较差。一氧化氮合酶的抑制剂未改变EtOH对AA诱导的聚集的抗聚集作用。另外，10 mM EtOH减少了血栓烷（Tx）的形成。在洗涤过的血小板中，1-10 mM EtOH部分抑制凝血酶诱导的血小板凝集。在洗涤后的静息血小板中，10 mM EtOH不会改变静息的[Ca ++] i，而会显着降低AA触发的[Ca ++] i的增加。离体实验的结果表明，葡萄酒会增加HDL。但是，该观察结果可能会或可能不会影响血小板对激动剂的反应。我们的研究结果表明，低剂量的酒精会降低血小板功能。

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