Lominadze D G, Saari J T, Miller F N, Catalfamo J L, Justus D E, Schuschke D A
Center for Applied Microcirculatory Research, University of Louisville, KY 40292, USA.
Thromb Haemost. 1996 Apr;75(4):630-4.
The role of dietary copper deficiency in platelet-to-endothelial cell adhesion and in platelet-to-platelet aggregation was studied in vitro. Platelets were obtained from male, weanling Sprague-Dawley rats fed purified diets which were either copper-adequate (CuA, 6.3 micrograms copper/g of diet) or copper-deficient (CuD, 0.3 microgram/g of diet) for 4 weeks. The platelet adhesion study was performed by adding CuA or CuD platelets either suspended in homologous plasma or in Tyrode buffer salt solution (TBSS) to cultured rate endothelial cells. After a one hour incubation at 37 degrees C non-adhered platelets were removed and counted in a microcytometer. Platelet aggregation in platelet rich plasma (PRP) samples was induced by adding ADP (2 x 10(-4)M) and measured in a turbidometric aggregometer. The content of von Willebrand factor (vWF) in platelets and in plasma and the content of fibrinogen in platelets was determined. Platelet adhesion to rat endothelial cells was significantly lower for platelets from CuD rats than for platelets from CuA rats. ADP induced platelet aggregation from CuD rats was significantly higher than platelet aggregation from CuA rats. The content of vWF in platelets and in plasma from CuD rats was significantly lower than in platelets and plasma from CuA rats. However, the amount of fibrinogen in platelets from ++CuD rats was about 4-fold higher than that in platelets from CuA rats while the plasma fibrinogen was lower in CuD rats than in CuA rats. These studies illustrate that copper deficiency diminishes platelet adhesion to endothelial cells but increases platelet aggregability. The results suggest that these physiological alterations may be the result of decreased platelet vWF and increased platelet fibrinogen during dietary copper deficiency.
在体外研究了膳食铜缺乏在血小板与内皮细胞黏附以及血小板与血小板聚集过程中的作用。从雄性断乳斯普拉格-道利大鼠获取血小板，这些大鼠被喂食纯化日粮4周，日粮分为铜充足组（CuA，每克日粮含6.3微克铜）和铜缺乏组（CuD，每克日粮含0.3微克铜）。血小板黏附研究通过将悬浮于同源血浆或泰罗德缓冲盐溶液（TBSS）中的CuA或CuD血小板添加到培养的大鼠内皮细胞中来进行。在37℃孵育1小时后，去除未黏附的血小板并在血细胞计数器中计数。通过添加ADP（2×10⁻⁴M）诱导富含血小板血浆（PRP）样本中的血小板聚集，并在比浊法血小板聚集仪中进行测量。测定血小板和血浆中血管性血友病因子（vWF）的含量以及血小板中纤维蛋白原的含量。与CuA大鼠的血小板相比，CuD大鼠的血小板对大鼠内皮细胞的黏附显著降低。ADP诱导的CuD大鼠的血小板聚集显著高于CuA大鼠的血小板聚集。CuD大鼠的血小板和血浆中vWF的含量显著低于CuA大鼠的血小板和血浆中的含量。然而，CuD大鼠血小板中的纤维蛋白原量比CuA大鼠血小板中的纤维蛋白原量高约4倍，而CuD大鼠血浆中的纤维蛋白原含量低于CuA大鼠。这些研究表明，铜缺乏会减少血小板与内皮细胞的黏附，但会增加血小板聚集性。结果表明，这些生理改变可能是膳食铜缺乏期间血小板vWF减少和血小板纤维蛋白原增加的结果。
