【摘要】 作者对照研究了20例CMPD患者和20例正常人的血小板功能,并观察了其中 13例患者和 8例正常人的血小板超微结构。发现CMPD患者血小板粘附功能与ADP、肾上腺素、胶原、瑞斯脱霉素所诱导的血小板聚集功能均降低,血小板内致密颗粒数减少。由此表明CMPD 患者具有血小板粘附与聚集功能障碍。作者认为这种功能障碍可能是导致患者出血和血栓形成的主要原因;但从本研究结果还看不出血小板功能变化与患者出血和血栓形成的临床表现之间有何平行关系。更多还原

【Abstract】 Control study of platelet adhesivenessand aggregations induced by ADP, epineph-rine, collagen and ristocetin in 20 patientswith CMPD and 20 healthy volunteerswas done. The platelets from thirteenpatients and the eight volunteers wereexamined by transmission electron micros-copy. The results showed that the plateletaggregation rates of the patients inducedby ADP, epinephrine, collagen were lowerthan those of the control group. Plateletadhesiveness of the patients was lowerthan that of the control group. Basing onour study, we are unable to demonstratea definite correlation between plateletfunction alteration and clinical bleedingor thrombosis. The electron microscopic examinationshowed that the number of dense body ofthe platelets in patients with CMPD waslower than those of the control, but theα-granule existed no significant differencebetween them. Our result confirms theexistence of storage pool deficiency inCMPD, which may account for the abnor-malities in platelet adhesiveness and ag-gregation. The platelet aggregation rate inducedby ristocetin was significantly lower in thepatients with CMPD, we speculate thatthe acquired von Willebrand’s diseasemight be one of the factors of bleedingin the CMPD patients.更多还原