血管性痴呆患者血小板活化机制的研究

STUDY ON MECHANISM OF PLATELET ACTIVATION IN VASCULAR DEMENTIA

为探讨血管性痴呆(VD)血小板活化机制 ,分别测定 32例VD患者、38例急性脑梗死(ACI)患者及 2 8名健康对照者血小板MLCK ,Ca2 + Mg2 + ATP酶活性和血小板 [Ca2 + ]i浓度。结果发现 ,与健康对照组相比 ,VD组和ACI组MLCK活性明显增加 (P <0 0 1) ,Ca2 + Mg2 + ATP酶活性明显降低 (P<0 0 5 ,P <0 0 1) ;VD组和ACI组血小板静息 [Ca2 + ]i均高于健康对照组并与MLCK活性呈显著正相关 (P <0 0 1) ,与Ca2 + Mg2 + ATP酶活性呈负相关 (P <0 0 5 )。提示 ,血小板MLCK和Ca2 + Mg2 + ATP酶活性以及血小板 [Ca2 + ]i浓度与血管性痴呆的发生有密切关系。

To explore the mechanism of platelet activateation in vascular dementia(VD), the activity of myosin light chain phosphorylation and Ca 2+ Mg 2+ ATPase,the concentration of [Ca 2+ ]i were measured in 28 healthy controls, 38 patients with acute cerebral infarction (ACI), and 32 patients with VD. The activity of MLCK in VD and ACI groups was significantly higher than that in the controls( P <0 01).The acitivities of Ca 2+ Mg 2+ ATPase were markedly lower than those of the controls( P <0 05, P <0 01).The static density of platelet [Ca 2+ ]i in VD and ACI patients was obviously higher than that of the controls( P <0 01). The static density of platelet [Ca 2+ ]i was positively correlated with the activity of MLCK( P <0 01) and negatively correlated with the activity of Ca 2+ Mg 2+ ATPase( P <0 05). These results suggest that the platelet function could be abnormal in VD and ACI patients, and the changes in activity of MLCK and Ca 2+ Mg 2+ ATPase and static density of platelet [Ca 2+ ]i might be involved in the process of molecular pathogenesis of VD.