Taketomi Y, Kuramoto A
Thromb Haemost. 1978 Aug 31;40(1):11-23.
Positively charged macromolecule, polylysine (mol. wt. 15,000; 23,000; 180,000) could induce the platelet aggregation in low concentration but high concentration was required in the case of neutral macromolecule, dextran (mol. wt. 40,000; 250,000; 2,000,000). The larger molecules of polylysine and dextran were more effective in inducing platelet aggregation. In the dextran-induced aggregation, positively charged Thorotrast particles on the cell surface did not decrease significantly. On the other hand, the surface membranes of platelets aggregated by polylysine were essentially devoid of bound particles. Heparin inhibited the polylysine-induced platelet aggregation but not the dextran-induced aggregation. These findings suggested that polylysine induced aggregation more effectively than dextran by reducing the negative surface charge and giving stronger adsorption force on cell surface. In platelet-rich plasma, polylysine elicited the release reaction of 14C-serotonin but dextran did not. Possible mechanism by which polylysine could elicit the release reaction is the formation of more tightly packed platelet aggregate than that by dextran in the presence of the low calcium ion concentration in citrated platelet-rich plasma. Average distance between plasma membranes of aggregated platelets, however, did not vary with the degrees of polymerization of these macromolecules.
带正电荷的大分子聚赖氨酸(分子量分别为15,000、23,000、180,000)在低浓度时就能诱导血小板聚集,而中性大分子右旋糖酐(分子量分别为40,000、250,000、2,000,000)则需要高浓度才能诱导血小板聚集。聚赖氨酸和右旋糖酐中较大的分子在诱导血小板聚集方面更有效。在右旋糖酐诱导的聚集中,细胞表面带正电荷的二氧化钍颗粒没有明显减少。另一方面,由聚赖氨酸聚集的血小板表面膜基本上没有结合颗粒。肝素抑制聚赖氨酸诱导的血小板聚集,但不抑制右旋糖酐诱导的聚集。这些发现表明,聚赖氨酸通过减少表面负电荷并在细胞表面产生更强的吸附力,比右旋糖酐更有效地诱导聚集。在富血小板血浆中,聚赖氨酸引发了14C-血清素的释放反应,而右旋糖酐则没有。聚赖氨酸引发释放反应的可能机制是,在枸橼酸化富血小板血浆中低钙离子浓度的情况下,聚赖氨酸比右旋糖酐形成了更紧密堆积的血小板聚集体。然而,聚集血小板质膜之间的平均距离并没有随着这些大分子的聚合度而变化。