摘要
目的 :研究补体激活对男性冠心病 (CHD)及健康成年人血小板的作用及抗CD5 9对该作用的影响。方法 :应用眼镜蛇毒因子 (CVF)活化血小板 ,通过测定男性CHD及健康成年人血小板的聚集及释放曲线 ,观察抗CD5 9应用前后CVF对血小板变形、聚集及释放功能的影响。结果 :CVF能诱导男性CHD及健康成年人血小板显著、持久的变形和释放 ,但不能诱导血小板聚集。当CVF浓度在 12 .5～ 5 0 .0g/L范围内 ,各组血小板的最大变形幅度与CVF浓度的对数呈线形相关 ,回归方程于CHD组 (36例 )为Y =2 8.717lgX - 19.798(r =0 .95 6 ,P<0 .0 1) ;健康成年人组为Y =2 6 .0 88lgX - 15 .5 81(r =0 .970 ,P <0 .0 1)。抗CD5 9能增强CVF诱导的血小板的最大变形幅度 ,并与剂量相关 ,其血小板最大变形幅度CHD组及健康成年人组分别为空白对照时的 1.39和1.36倍 (P <0 .0 1)。同时抗CD5 9也促进补体诱导的血小板ATP分泌增多。但两组间血小板对CVF及抗CD5 9的反应差异无统计学意义。结论 :活化的补体能诱导男性CHD及健康成年人血小板发生变形、释放 ,但不诱导血小板的聚集 ,且抗CD5
Objectives: To study the reactions of human platelet to active complement and the effects of anti-CD59 on platelet activation induced by complement in patients with coronary heart disease (CHD) and healthy adult males. Methods: By applying CVF to activate complement, observed the platelet aggregation and release reactions with or without applying anti-CD59 to block the complement modulation protein CD59 in CHD and healthy men. Results: CVF could induce platelet release and occur significant and lasting metamorphosis in CHD and healthy individuals, but failed to induce platelet aggregation. In the two groups, CVF-induced platelet metamorphosis showed positive linear correlation to lg concentration of CVF. The regressive equations were Y= 28.717 lgX- 19.798 (r= 0.956,P< 0.01, n=36) in CHD group, and in healthy group Y= 26.088 lgX- 15.581 (r= 0.970,P< 0.01, n=36). Anti-CD59 could enhance CVF-induced platelet shape change with a dose-dependent manner in the two groups. The maximum enhancive ratios of platelet shape change were 1.39 and 1.36 in CHD group and healthy group respectively(P< 0.01). Anti-CD59 also could enhance platelet ATP release induced by CVF. Conclusions: Complement activated by CVF can induce significant and lasting platelet metamorphosis and release reaction, but can not induce platelet aggregation in CHD and healthy adult males. Anti-CD59 can promote the platelet reactions induced by active complement.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2004年第1期4-6,共3页
Journal of Clinical Cardiology
