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血小板激活及血小板参数变化在脑梗死发病机制中的作用
引用本文:周红,施咏梅,刘韶华. 血小板激活及血小板参数变化在脑梗死发病机制中的作用[J]. 临床神经病学杂志, 2006, 19(1): 18-21
作者姓名:周红  施咏梅  刘韶华
作者单位:210009,南京,东南大学附属中大医院神经内科;210009,南京,东南大学附属中大医院神经内科;210009,南京,东南大学附属中大医院神经内科
摘    要:目的研究血小板激活以及血小板参数变化在脑梗死发病机制中的作用。方法采用流式细胞术测定急性脑梗死患者168例和健康对照者40名外周血P选择素(CD62p)、溶酶体蛋白(CD63)的阳性表达率,同时测定血小板计数(PLT)、血小板平均体积(MPV)和血小板最大聚集率(MAR)。并进行比较及相关因素分析。结果(1)脑梗死患者CD62p、CD63及MPV、MAR明显高于健康对照组,并且上述指标急性期均高于恢复期(均P<0·01);(2)全前循环梗死(TACI)亚型的脑梗死患者CD62p、CD63及MPV、MAR显著高于部分前循环梗死(PACI)、后循环梗死(POCI)及腔隙性梗死(LACI)亚型,在PACI及POCI亚型中上述各测定值较LACI亚型显著增高,差异均具有显著性(均P<0·01);而在PACI及POCI亚型之间差异并无显著性(P>0·05);(3)PLT在脑梗死患者急性期、恢复期与健康对照组之间以及牛津郡社区卒中项目(OCSP)各亚型之间差异无显著性(均P>0·05)。(4)CD62p、CD63呈显著正相关(r=0·826,P<0·01),且与MPV及MAR亦呈明显正相关(r=0·703、0·698,均P<0·01);但与PLT之间无相关性(均P>0·05)。结论脑梗死患者血小板的大量激活及其体积和最大聚集率的升高参与了脑梗死的病理过程,监测MPV和MAR较PLT更能反映脑梗死的病情程度,为应用抗血小板聚集药物提供依据。

关 键 词:脑梗死  P选择素  溶酶体膜蛋白  血小板  流式细胞术
文章编号:1004-1648(2006)01-0018-04
收稿时间:2005-02-06
修稿时间:2005-11-11

Role of platelet activation and changes of platelet parameters in the pathogenesia of cerebral infarction
ZHOU Hong,SHI Yong-mei,LIU Shao-hua. Role of platelet activation and changes of platelet parameters in the pathogenesia of cerebral infarction[J]. Journal of Clinical Neurology, 2006, 19(1): 18-21
Authors:ZHOU Hong  SHI Yong-mei  LIU Shao-hua
Affiliation:Department of Neurology, Zhongda Hospital, Southeast University, Nanjing 210009, China
Abstract:Objective To investigate the role of platelet activation and the changes of platelet parameters in the pathogenesis of cerebral infarction.Methods Platelet activation factor P-selectin (CD62p), lysosomal membrane protein53(CD63 )were detected by flow cytometry and the three parameters [platelet count (PLT), mean platelet volume (MPV)and maximum platelet aggregation rate (MAR)] were measured in 168 patients with cerebral infarction and 40 normal controls. Results (1) The positive rates of CD62p, CD63 and the levels of MPV, MAR in patients with cerebral infarction were significantly higher than those in control group (all P< 0.01). Moreover these indexes in acute phase were higher than those in convalescence after cerebral infarction (all P< 0.01). (2) The positive rates of CD62p, CD63 and the levels of MPV, MAR were obviously higher in total anterior circulation infarct (TACI ) subtype than that of in partial anterior circulation infarction (PACI), posterior circulation infarct (POCI) and Lacunar infarction (LACI) subtype (all P< 0.01), those in PACI and POCI subtype were markedly higher than in LACI subtype ( P< 0.01), but there was no significant difference between PACI and POCI subtype ( P> 0.05). (3) No significant difference in PLT was found in all these groups or Oxfordshire Community Stroke Project (OCSP) subtypes(all P> 0.05).(4) There was significant correlation between CD62p and CD63 ( P< 0.01). The expression of CD62p and CD63 were closely associated with MPV or MAR (all P< 0.01), but they were not correlated to the PLT (all P> 0.05). Conclusions Patients with cerebral infarction show evidence of enhanced platelet activation and increasment of MPV and MAR,which may relate to the pathological process of cerebral infarction. Moreover MPV and MAR can reflect the clinical severity of cerebral infarction better than PLT. Anti-platelet aggregation treatment should be further taken in patients with cerebral infarction.
Keywords:cerebral infarction  P-selectin  lysosomal membrane protein53  platelet  flow cytometry
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