Zhao B, Filler T J, Rickert C H, Dierichs R
Platelet Research Unit, University of Münster, Germany.
Cell Tissue Res. 1995 Apr;280(1):183-8. doi: 10.1007/BF00304523.
The adhesion of human blood platelets is studied with an in vitro model using reflection contrast microscopy and an image analysis system. The adhesive feature is promoted by oxidatively modified low density lipoprotein, which also induces functional morphological changes of platelets. However, when washed platelets are pretreated with 0.05 mM cytochalasin D, oxidized low density lipoprotein (100 micrograms/ml) causes a slower increase of the adhesion area (11.6 microns 2/min) compared to untreated platelets (15.7 microns 2/min) or platelets treated by oxidized low density lipoprotein alone (20.5 microns 2/min, P < 0.01). These results are supported by light transmission analysis and by transmission electron microscopy. Our experiments suggest that cytochalasin D inhibits the change of platelets in shape induced by oxidized low density lipoprotein, hinders the adhesion, but does not prevent the adhesion entirely.
利用反射对比显微镜和图像分析系统的体外模型研究了人血小板的黏附。氧化修饰的低密度脂蛋白促进了黏附特性，其还诱导血小板的功能形态变化。然而，当用0.05 mM细胞松弛素D预处理洗涤过的血小板时，与未处理的血小板（15.7平方微米/分钟）或仅用氧化低密度脂蛋白处理的血小板（20.5平方微米/分钟，P<0.01）相比，氧化低密度脂蛋白（100微克/毫升）导致黏附面积的增加较慢（11.6平方微米/分钟）。这些结果得到了光透射分析和透射电子显微镜的支持。我们的实验表明，细胞松弛素D抑制氧化低密度脂蛋白诱导的血小板形状变化，阻碍黏附，但不能完全阻止黏附。
