血清Lipoprotein(a)濃度の血小板凝集能, 粘着能におよぼす影響

• Published in: 動脈硬化 Vol. 25; no. 9-10; pp. 341 - 345
• Main Authors: 布施川, 雄一, 玉地, 寛光, 半田俊, 之介, 後藤, 俊哉
• Format: Journal Article
• Language: Japanese
• Published: 一般社団法人 日本動脈硬化学会 15.07.1998; Japan Atherosclerosis Society
• Subjects: Anti Glycoprotein IIb; IIIa antibody; Laser light scattering; Lipoprotein (a); Platelet aggregates; Platelet aggregation
• ISSN: 0386-2682; 2185-8284
• DOI: 10.5551/jat1973.25.9-10_341

Although some investigations reported that there is an interaction between lipoprotein (a) and resting platelets, no reports have been published on the relationship between lipoprotein (a) and platelet adhesion or aggregation in clinical study. We measured plasma lipoprotein (a) concentration and platelet function in 100 normal volunteers and 81 patients with type ha and 41 patients with type IV non familial hyperlipidemia. Platelet aggregation were measured by Bom's method using optical density, and platelet small, median and large aggregates were detected by newly developed system using laser light scattering. In healthy females, subjects with high lipoprotein (a) concentration showed higher counts of platelet small aggregates formed in absence of chemical stimulants than subjects with low lipoprotein concentration (p<0.05). In the patients with type IV hyperlipidemia, patients with high lipoprotein (a) concentration showed higher counts of large aggregates formed by 1μM of ADP than patients with low lipoprotein (a) concentration (p<0.05). In patients with type IV, patients with high platelet aggregability induced by epinephrine showed higher lipoprotein (a) concentration than patients with low aggregability (p<0.05), and in healthy females, subjects with high platelet aggregabilitry induced by ADP showed higher lipoprotein (a) concentration than subjects with low aggregability (p<0.05). In the healthy males and the patients with type ha hyperlipidemia, there was no significant difference in platelet aggregability between high and low concentration of lipoprotein (a) group. In high lipoprotein (a) concentration, washed platelets by HEPES buffer increased the formation of platelet small, median and large aggregates induced by 3μM of ADP. Platelet small aggregates formed spontaneously were inhibited by monoclonal anti GPIIb/IIIa antibody but not by monoclonal anti GPIb antibody. It was suggested that lipoprotein (a) influences on platelet aggregation in healthy female and the patients with type IV hyperlipidemia. But this mechanism is unclear. Further investigation seemed to be necessary.