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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 9能增强补体诱导的血小板功能改变
Objective: To study the effect of complement activation on platelets in male patients with coronary heart disease (CHD) and healthy adults and the effect of anti-CD5 9 on this effect. Methods: Platelets were activated by cobra venom factor (CVF). The platelet aggregation and release profiles of male CHD and healthy adults were measured. The effects of anti-CD5 9 on platelet deformity, aggregation and release were observed. RESULTS: CVF induced significant and sustained platelet deformity and release in CHD and healthy adults but not platelet aggregation. When the concentration of CVF was in the range of 12.5 ~ 5.0 g / L, the maximum amplitude of platelet deformation was linearly correlated with the logarithm of CVF concentration. The regression equation was linear in the CHD group (36 cases) as Y = 2 8.717 lgX - 19.798 (r = 0.956, P <0.01). The healthy adult group was Y = 26.088lgX - 15.581 (r = 0.970, P <0.01). Anti-CD5 9 enhanced the maximum amplitude of CVF-induced platelet deformity, and was dose-dependent. The maximum platelet deformity of CHD group and healthy adult group were 1.39 and 1.36 times higher than that of blank control group (P <0.01). At the same time anti-CD5 9 also promote complement-induced increase in platelet ATP secretion. However, there was no significant difference in the response of platelets to CVF and anti-CD59 between the two groups. CONCLUSION: Activated complement can induce platelet deformity and release in CHD and healthy adults without inducing platelet aggregation, and anti-CD59 enhances complement-induced platelet function changes