血小板活化指标与短暂性脑缺血发作的转归

目的探讨短暂性脑缺血发作(TIA)患者疾病转归与血小板活化指标α颗粒膜糖蛋白(CD62p)、溶酶体颗粒膜糖蛋白(CD63)、血小板膜表面糖蛋白(CD41)的关系.方法57例TIA患者随访2个月,分别在服药后1 d、1周、1个月和2个月时采用流式细胞仪检测血小板CD62p、CD63和CD41表达的百分率,同时监测病情发展趋向.结果TIA缓解组、TIA反复发作组与TIA进展为脑梗死组的血小板CD62p、CD63、CD41阳性百分率逐级升高(P＜0.05～＜0.001),尤其以进展为脑梗死组指标升高最为明显(P＜0.01～0.001).结论血小板活化CD62p,CD63及CD41可作为TIA发展演变的估测指标.     

氯吡格雷与阿司匹林联合应用在急性脑梗死治疗中的疗效评定

目的观察急性脑梗死患者血小板上α颗粒膜糖蛋白(CD62p)及溶酶体颗粒膜糖蛋白(CD63)的表达,通过血小板活化的变化,探讨阿司匹林与氯吡格雷联合用药与阿司匹林单药治疗的疗效差异。方法将60例脑梗死患者随机分为两个亚组:单药组(阿司匹林0.15 g/d)和联合用药组(阿司匹林0.10 g/d+氯吡格雷75 mg/d),30例健康体检者为对照组。使用流式细胞术检测所有病例CD62p、CD63阳性率,对单药组和联合用药组治疗前后的CD62p、CD63阳性率进行比较,同时进行NIHSS评分。结果脑梗死组血小板CD62p、CD63阳性率显著高于对照组(P<0.01)。单药组和联合用药组在治疗一周和二周后CD62p、CD63阳性率和NIHSS评分均较治疗前显著下降(P<0.01)。联合用药组治疗二周后与单药组比较CD62p、CD63阳性率和NIHSS评分明显降低,差异有统计学意义(P<0.01)。结论抗血小板治疗对脑梗死有效,阿司匹林+氯吡格雷联合治疗的总体疗效明显优于单用阿司匹林,CD62p、CD63可以衡量抗血小板治疗效果。     

不同剂量阿司匹林在急性脑梗死治疗中的疗效比较

目的 通过观察急性脑梗死患者α颗粒膜糖蛋白(CD62p)及溶酶体颗粒膜糖蛋白(CD63)表达水平,探讨以血小板活化的变化反映不同剂量阿司匹林的疗效差异.方法 使用流式细胞术检测阿司匹林0.15 g、0.20 g治疗前后的CD62p、CD63阳性率,同时进行NIHSS评分.结果 脑梗死组血小板CD62p、CD63阳性率显著高于对照组(P＜0.01),其在阿司匹林治疗前后也有显著差异(P＜0.01),但是阿司匹林0.15 g组与0.20 g组间比较无显著性差异,两个剂量组疗效比较无差异.结论 阿司匹林治疗脑梗死有效,但是其0.15 g与0.20 g剂量的疗效可能无明显差异.     

TIA患者血小板活化功能的变化及奥扎格雷对其影响

目的 探讨TIA患者血小板活化功能的变化及奥扎格雷对其影响.方法 应用流式细胞仪和单克隆抗体技术测定丹参治疗组和奥扎格雷治疗组不同时段的颗粒膜蛋白140(CD62p)、溶酶体整合膜糖蛋白(CD63)值.结果 TIA患者血小板表达CD62p、CD63明显增高,经奥扎格雷治疗后CD62p、CD63快速下降,较丹参治疗组有显著差异(P<0.01).结论 血小板表达CD62p、CD63在TIA患者中明显增强,并与病情转归相关;奥扎格雷干预治疗可使CD62p、CD63快速下降,提高治疗的有效率.     

脑血管病患者血小板膜糖蛋白测定的临床意义

目的　探讨脑血管病患者血小板膜糖蛋白测定的临床意义。方法　采用流式细胞仪测定 5 4例脑血管病患者及 2 0名正常对照者外周血血小板活化分子标记物颗粒蛋白 (GMP) CD6 2 p,CD6 3;整合数 α b链 (CD4 1b) ;血小板膜糖蛋白 Gp Ib(CD4 2 b)。结果　脑梗死患者 CD6 2 p、CD6 3的阳性率明显高于健康对照组及脑出血组 (P<0 .0 1)。而脑梗死组发病 3天以内的 CD6 2 p、CD6 3阳性率较发病 2 0天以上者显著增高 (P<0 .0 1)。但后者仍高于健康对照组 (P<0 .0 1) ,CD4 1b、CD4 2 b在各组间无显著差异。结论　脑梗死患者的血小板活化程度明显增高 ,尤其是 CD6 2 p、CD6 3。提示阻止或抑制血小板活化的途径将是防治脑梗死的方法之一     

血小板膜糖蛋白在新疆汉族及哈萨克族脑梗死患者中表达的差异及临床探讨

目的探讨血小板膜糖蛋白a-颗粒膜蛋白(CD62p)在新疆汉族及哈萨克族脑梗死患者表达上的差异情况及临床意义。方法将汉族及哈萨克族脑梗死患者各80例分成两组,并设立两种民族健康对照组100例。用流式细胞仪检测CD62p的表达率。结果脑梗死组CD62p表达均显著高于健康对照组,汉族脑梗死及哈萨克族脑梗死之间亦有差异。结论脑梗死患者血栓的形成与血小板活化密切相关。     

糖尿病性腔隙性脑梗死患者细胞黏附分子表达的观察

目的 :探讨血糖对黏附分子的影响及其在LI发病机制中的作用。方法 :采用流式细胞术对LI合并Ⅱ型糖尿病及非糖尿病LI病人外周血白细胞的膜糖蛋白CD11b、CD18和血小板膜糖蛋白CD62p的表达进行检测。结果 :两组病人比较血小板膜糖蛋白CD62p、白细胞膜糖蛋白CD11b、CD18表达在腔隙性脑梗死合并糖尿病组明显高于非糖尿病腔隙性脑梗死组 ;血糖与CD62p、CD11b呈正相关 ;CD62p、CD11b、CD18及血糖与LI腔梗个数无关。结论 :超负荷血糖时血小板、白细胞均处于高活化状态。超负荷血糖导致的细胞黏附分子的高表达参与LI微血管病变的损伤过程。     

脑血管疾病患者血小板的活化状态变化分析

目的探讨脑血管疾病患者血小板的活化状态变化的临床意义。方法随机选择90例脑血管疾病患者,其中脑梗死(脑梗死组)和高血压(高血压组)患者各45例,并选择30例健康者为对照组。利用流式细胞仪检测所有研究对象的血小板活化状态,并进行比较。结果脑梗死组和高血压组的血小板表面膜糖蛋白CD41、CD61较对照组差异无统计学意义(均P0.05);但较健康对照组,血小板表面膜糖蛋白CD62p、CD63均出现显著上升的情况,差异均有统计学意义(均P0.05)。结论脑血管疾病患者的血小板活化状态显著增强,临床对血小板表面膜糖蛋白的检测具有重要意义。     

氯吡格雷联合奥扎格雷钠治疗急性缺血性卒中疗效评价

研究背景抗血小板治疗已经成为缺血性卒中的常规治疗方法,目前对其作用的肯定主要源于临床应用,迄今尚无一项能够准确评价其有效性的实验室指标。有研究证实,血小板活化程度与动脉粥样硬化和缺血性卒中相关,尤其是血小板α颗粒膜糖蛋白CD62p和溶酶体膜糖蛋白CD63均为血小板活化的重要指标。本研究旨在通过观察急性缺血性卒中患者血小板膜表面CD62p和CD63表达变化,探讨以血小板活化程度反映氯吡格雷(75 mg)、奥扎格雷钠(80 mg)与阿司匹林(0.15 g)的疗效差异。方法采用流式细胞术检测急性缺血性卒中患者氯吡格雷(75 mg)联合奥扎格雷钠(80 mg,联合治疗组)及阿司匹林单药(阿司匹林组)治疗前后血小板CD62p和CD63阳性表达率,美国国立卫生研究院卒中量表(NIHSS)评价神经功能改善程度。结果与正常对照组相比,治疗前急性缺血性卒中组患者血小板CD62p和CD63阳性表达率升高(P=0.001,0.032);治疗后CD62p和CD63阳性表达率、NIHSS评分逐步下降(均P=0.000)。与治疗前相比,治疗后联合治疗组和阿司匹林组患者血小板CD62p和CD63阳性表达率、NIHSS评分逐步下降(均P=0.000),但组间差异无统计学意义(均P>0.05)。CD62p和CD63阳性表达率在不同观察时间点与治疗分组之间不存在交互作用(F=1.403,P=0.250;F=2.830,P=0.063),但NIHSS评分在不同观察时间点与治疗分组之间存在交互作用(F=4.518,P=0.013)。结论抗血小板药物治疗急性缺血性卒中有效,但氯吡格雷与奥扎格雷钠联合治疗之疗效与阿司匹林单药治疗并无差异。缺血性卒中急性期测定血小板CD62p阳性表达率可以用于评价抗血小板药物的疗效,但CD63表达的临床价值尚待进一步研究。     

CD62p、CD63联合血栓弹力图检测在氯吡格雷治疗复发性脑梗死的临床意义

目的 探讨初发脑梗死患者与复发脑梗死患者在氯吡格雷治疗后,血小板膜糖蛋白CD62p、CD63及血栓弹力图指标变化特点及其临床意义。方法 纳入2019年7月至2021年1月在该院住院的急性缺血性脑卒中患者103例,分为复发脑梗死组（43例）和初发脑梗死组（60例）。入院后服用氯吡格雷(75 mg/d),服药后第8天采用流式细胞术测定患者血浆中血小板膜糖蛋白CD62p和CD63表达率,并行血栓弹力图(TEG)检测,包括血小板ADP抑制率(%)、血细胞凝集块形成时间(K)、凝血反应时间(R)、血细胞凝集块形成速率(α角)和血凝块最大硬度或强度(MA)等指标,分析TEG各参数与CD62P、CD63表达率特点及其相关性。结果 初发组和复发组治疗后血小板糖蛋白CD62p、CD63表达阳性率较治疗前均下降,差异具有统计学意义(P<0.05)。与初发组相比,复发组治疗后CD62p、CD63的表达阳性率下降幅度更小,差异具有统计学意义(P<0.05)。与初发组相比,复发组治疗后第8天检测血小板ADP抑制率更低、K值更短、MA更高,差异具有统计学意义(P<0.05)。初发组与复发组治疗第8天TEG检测中凝血反应时间R与CD63表达阳性率均呈负相关;CD62p表达阳性率与ADP抑制率均呈负相关。复发组ADP抑制率与CD63表达阳性率呈负相关。结论 复发性脑梗死患者在氯吡格雷治疗后具有更高的血小板反应性、血小板活性和血凝状态,CD62p、CD63联合血栓弹力图指标检测有一定的临床意义。引用格式:471-475.]     

Blood platelet activation markers in patients with acute cerebral infarction during the earliest stage of the disease--evaluation using flow cytometry methods

Platelet activation seems to play a critical role in a number of vascular diseases, including stroke. The aim of our study was whole-blood flow cytometry evaluation of platelet activation markers: P-selectin (CD62), glycoprotein-53 (CD63) and platelet-derived microparticle in vivo in patients with acute cerebral infarction. We investigated 50 patients (29 men and 21 women, mean age 67.8) with acute cerebral infarction. Parameters of platelet activation were measured on the 1st, 3rd and 7th day after stroke onset. Comparisons were made with 20 control patients matched age. Compared to controls (1.6 +/- 0.7%) the stroke patients showed higher expression of CD62 on the 1st (2.6 +/- 1.4%), 3rd (3.5 +/- 2.3%) and 7th (3.0 +/- 2.0%) day after stroke onset. The differences were statistically significant on all days (p < 0.05). Compared to controls (1.5 +/- 0.6%) the stroke patients had also higher expression of CD63 on the 1st (1.9 +/- 0.6%), 3rd (2.0 +/- 0.6%) day and they showed higher level of platelet-derived microparticles on the 3rd (13.0 +/- 3.0%) day after stroke onset. The differences were statistically significant (p < 0.05). Elevated expression of CD62, CD63 and platelet-derived microparticles level indicate platelet activation during the acute phase of ischaemic stroke. Flow cytometry is a useful tool for in vivo assessment of platelet activation.     

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

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。     

脑梗死患者血浆ICAM-1、CD62p、CD63的动态变化及其临床意义

目的 探讨脑梗死患者血浆细胞间黏附分子（ICAM-1）、血小板表面P选择素（CD62p）、溶酶体颗粒糖蛋白53（CD63）的动态变化及其临床意义。方法 用流式细胞仪观察60例脑梗死患者发病3d、7d、14d外周血中ICAM-1、CD621，CD63的变化，并与20名健康者进行比较。结果 脑梗死3d、7d上述3项指标明显高于14d及正常对照组（均P〈0．05），而3d与7d间则差异不显著（P〉0．05）；ICAM-1与CD62p、CD63间无相关关系（r=0．1385、0．1632，均P〉0.05）；CD62p与CD63呈显著正相关（r=0.746，P〈0．05）；3项指标与临床神经功能缺损程度评分无相关性（r=0.1462、0.2145、0．368，均P〉0．05）。结论 脑梗死后ICAM-1表达增强，介导了粒细胞与脑血管内皮发细胞间的黏附，同时血小板表面CD62p、CD63表达增强，反映了血小板的活化程度与功能状态，评介导了血小板与中性粒细胞及内皮细胞间的黏附，促进了脑梗死的发生和发展，加重了脑组织的损伤。     

缺血性脑卒中患者P选择素、溶酶体蛋白表达的变化及其临床意义

目的　探讨缺血性脑卒中患者P选择素(CD62P)、溶酶体蛋白(CD63)表达的规律及其临床意 义。方法　运用流式细胞术检测168例缺血性脑卒中患者(急性期及恢复期)及40名健康对照者CD62P、CD63 的表达,并与神经功能缺损程度评分(NDS)进行相关分析。结果　(1)缺血性脑卒中患者急性期CD62P、CD63 表达[(9.48±1.24)%、(8.36±1.18)%]显著高于其恢复期[(5.73±1.27)%、(4.21±1.20)%]及健康对 照组[(1.59±0.56)%、(0.92±0.38)%](均P<0.01),恢复期CD62P、CD63表达仍高于对照组(P<0.01); (2)缺血性脑卒中组急性期患者按牛津郡社区卒中计划分为4个亚型,CD62P、CD63表达在完全前循环梗死 (TACI)组[(16.45±1.13)%、(15.59±1.28)%]明显高于部分前循环梗死(PACI)组[(10.63±1.18)%、 (9.38±1.14)%]、后循环梗死(POCI)组[(10.54±1.14)%、(9.33±1.13)%]及腔隙性梗死(LACI)组 [(6.59±1.35)%、(5.53±1.20)%](均P<0.01),PACI组及POCI组明显高于LACI组(均P<0.01),而 PACI组及POCI组之间差异无显著性(P>0.05);(3)CD62P、CD63表达与NDS呈显著直线正相关(r=0.84、 r=0.817,均P<0.01)。结论　缺血性脑卒中患者急性期CD62P、CD63表达显著升高,可能参与了缺血性脑损 伤形成的病理过程,并间接反映其病情程度;恢复期CD62P、CD     

伴高血压、糖尿病的脑梗死患者血小板活化水平与意义

目的观察伴高血压和／或糖尿病的脑梗死惠者血小板活化水平的变化,探讨其在疾病发生中的作用与意义。方法采用流式细胞术测定40例健康对照组和352例急性脑梗死惠者血小板活化指标CD62P、CD63的水平,同时对脑梗死患者按伴发疾病不同,分为高血压组、糖尿病组、高血压并糖尿病组,然后进行组间比较。结果脑梗死患者血浆CD62P、CD63水平明显高于对照组（P〈0.001）;高血压并糖尿病组脑梗死患者血浆CD62P、CD63水平明显高于高血压组（P〈0.01）;但与糖尿病组比较无显著差异（P〉0.05）;糖尿病组CD64P水平明显高于高血压组（P〈0.05）,而CD63水平比较无统计学差异（P〉0.05）。结论急性脑梗死早期活化血小板水平明显增高,伴有糖尿病及高血压并糖尿病的脑梗死患者活化血小板水平增高更加显著。     

Lack of uniform platelet activation in patients after ischemic stroke and choice of antiplatelet therapy

INTRODUCTION: Platelets play an important role in the natural history of ischemic stroke, and are known to be activated in the acute phase. Although aspirin reduces risks of myocardial infarction, stroke and cardiovascular death, the extent of platelet action and the effect of aspirin on platelet function in patients recovering from stroke remain unclear. METHODS: We studied 120 individuals divided into three equal groups: aspirin-free patients after ischemic stroke, post-stroke patients receiving aspirin (81-650 mg/daily), and aspirin-free subjects with multiple risk factors for vascular disease. Conventional platelet aggregation induced by 5 microM ADP and 5 microM epinephrine, cartridge-based analyzers (Ultegra, and PFA-100) readings, and expression of CD31, CD41a, CD42b, GPIIb/IIIa activity, CD51/CD61, CD62p, CD63, CD107a, CD154, CD165, formation of platelet-monocyte aggregates, intact (SPAN12), and cleaved (WEDE15) PAR-1 thrombin receptors by flow cytometry were analyzed. RESULTS: There were no differences between aspirin-free post-stroke patients and aspirin-free controls. Although aggregation was slightly higher, 12 out of the 14 receptor analyses, were surprisingly lower in the post-stroke cohort. Aspirin-treated patients exhibited highly significant inhibition of epinephrine-induced aggregation (p=0.0001), prolongation of the closure time (p=0.03), and reduction of the aspirin reactive units (p=0.02) measured by the Ultegra device. In addition, surface platelet expression of thrombospondin (p=0.001), GPIIb/IIIa activity (p=0.04), P-selectin (p=0.03), CD40-ligand (p=0.04), CD165 (p=0.02), the formation of the platelet-monocyte aggregates (p=0.01), and intact epitope of PAR-1 thrombin receptor (p=0.03) were significantly lower in the aspirin-treated group. CONCLUSIONS: Platelets are not activated in aspirin-free patients after ischemic stroke. Platelet function is significantly inhibited in those treated with aspirin when compared with healthy subjects with risk factors for vascular disease. Bleeding complications and hemorrhagic transformations after aggressive antiplatelet regimens could be related to the decreased or normal baseline platelet characteristics in such patients. Further analysis of platelet heterogeneity and its clinical significance remains to be determined in randomized trials.     

脑出血患者血小板CD42b、CD62p的表达及临床意义

目的研究脑出血急性期血小板表面糖蛋白CD42b、CD62p的表达及其与血肿周围脑水肿形成的关系。方法20例中等量脑出血患者,利用流式细胞仪(FCM)测定其血小板CD42b和CD62p的表达,并根据头颅CT测量血肿周围脑水肿带的大小,对两者进行相关性分析。结果与正常健康人比较,脑出血急性期血小板CD42b的表达减少,CD62p的表达增加;血小板CD42b、CD62p表达量与血肿周围脑水肿带的大小有相关性(rCD42b=-0.489,P<0.05;rCD62p=0.646,P<0.01)。结论脑出血急性期血小板活化,活化的血小板可能参与了血肿周围脑水肿形成这一病理损伤过程。     

Platelet activation in acute, decompensated congestive heart failure

BACKGROUND: Congestive heart failure (CHF) is associated with increased risk of venous thromboembolism, stroke and sudden death. This may be related to abnormalities of thrombogenesis and platelet activation. A comprehensive assessment of platelet (dys)function in acute decompensated heart failure (AHF) is lacking, and we hypothesised that such patients would show greater abnormalities in platelet indices, compared to stable CHF and healthy controls. METHODS: We measured soluble P-selectin (sP-sel, by ELISA); platelet surface P-selectin (CD62P%G) and CD63%G expression by flow cytometry; and platelet structural indices [mean platelet volume (MPV), mean platelet mass (MPM) and mean platelet component (MPC)] in 22 patients with AHF (pre- and posttreatment), who were compared to 68 patients with stable congestive heart failure (CHF, all with left ventricular ejection fraction (LVEF) <50%) and 23 healthy controls. RESULTS: There were significant differences between the 3 study groups in MPV (p<0.001), MPC (p=0.001), platelet surface P-selectin (CD62P%G, p<0.0001) and platelet surface CD63P%G (p=0.017). On post-hoc analyses, AHF patients had higher platelet surface P-selectin (CD62P%G) compared to stable CHF patients and healthy controls (Tukey's test, all p<0.05), whilst CD63%P was similarly high in both disease groups, compared to healthy controls. Platelet surface P-selectin (p=0.032), CD63 (p=0.024) and CD40L (p=0.024) were significantly reduced following treatment of AHF, though platelet morphology and sP-sel levels were not significantly changed. CONCLUSION: AHF patients demonstrate some abnormalities of platelet activation compared to stable CHF patients and healthy controls. These platelet abnormalities are modified by treatment, raising the possibility that platelets may partly contribute to the pathophysiology of adverse complications associated with AHF.     

血小板活化与多梗死性痴呆的关系研究

目的　探讨血小板活化与多梗死性痴呆 (MID)的关系。方法　采用流式细胞免疫技术 ,以抗血小板单克隆抗体及钙离子荧光剂为分子探针 ,检测了 4 6例MID患者的血小板CD62p、CD63 、P10 及红细胞内钙离子 (IECa2 + )含量 ,并与非血管性痴呆、急性脑梗死患者及健康人对比。结果　MID组CD62 p、CD63 、P10 及IECa2 + 均明显高于非血管性痴呆组及对照组 (P <0 .0 5 ,P <0 .0 1) ;低于急性脑梗死组 ,但无统计学意义 (P>0 .0 5 )。急性脑梗死组的四项指标也明显高于非血管性痴呆组 (P <0 .0 1)。在MID组CD62p、CD63 、P10 及IECa2 + 含量变化与病情、痴呆、智能相关 ,痴呆及智能评分较低者 ,上四项指标增高显著 ,二者呈负相关。结论　血小板活化、血小板活化因子含量变化是导致Ca2 + 稳态失调的重要因素 ,与MID的发生发展密切相关。