两种血小板聚集分析仪检测结果的分析比较

目的 通过PL-11血小板分析仪(结果用最大聚集率,maximum aggregation rate,PL-MAR％表示)与光比浊法血小板聚集仪(light transmittance aggregometry,LTA,结果用血小板最大聚集率,LTA-MAR％表示)检测结果的比较分析,探讨两种方法的优略.方法 利用二磷酸腺苷(adenosine phosphate,ADP)诱导LTA的血小板聚集实验,ADP诱导PL-11血小板分析仪的血小板聚集实验.结果 ①对照组与患者组对比,LTA-MAR％,PL-MAR％参数有统计学差异(P＜0.01);②PL-MAR％与LTA-MAR％呈正相关(r=0.889).结论 ①氯吡格雷有抗血小板聚集的药物效果.②PL-11作为一种新型的血小板分析仪,检测结果与LTA检测结果相关性好,精密度高,可作为血小板聚集功能检测的新途径.     

血小板聚集功能和尿11-脱氢血栓素B_2水平测定对评价脑梗死患者阿司匹林治疗作用的价值

目的:探讨血小板聚集功能和尿11-脱氢血栓素B2(11-DTB2)检测对评价一次及反复脑梗死患者服用阿司匹林治疗作用的价值。方法:42例反复脑梗死(≥2次)患者和50例发生一次脑梗死患者服用阿司匹林(100mg/天)至少7天后,用二磷酸腺苷(ADP)和花生四烯酸(AA)作诱导剂,测定两组血小板最大聚集率,并测定其11-DTB2的含量。结果:AA作诱导剂时,反复脑梗死患者与一次脑梗死患者比较,其血小板最大聚集率、阿司匹林半抵抗发生率明显较高(P<0.01);尿11-DTB2也是前者高于后者,差异有显著性统计学意义(P<0.01)。结论:脑梗死患者服用阿司匹林时检测血小板聚集功能和尿11-DTB2水平,可以观察阿司匹林抑制血小板功能的程度及临床疗效。     

急性心肌梗死后焦虑抑郁对血小板活性及疗效的影响

目的:探讨急性心肌梗死(AMI)后焦虑抑郁对血小板活性及抗血小板治疗效果的影响。方法:回顾性分析心肌梗死稳定期患者148例病例资料,均规律服用氯吡格雷75mg/d、阿司匹林100mg/d联合抗血小板治疗,发放汉密顿焦虑量表(HAMA)和汉密顿抑郁量表(HAMD)评估焦虑抑郁情况,并分析其对血小板活化、5-羟色胺(5-HT)及氯吡格雷疗效的影响。结果:焦虑和抑郁组初中及以下学历的几率分别为69.23%、76.47%高于非焦虑组的43.44%和非抑郁组的44.27%,差异均有统计学意义(χ~2=5.711,6.249;P0.05);非焦虑组CD62p、PAC-1、血小板聚集率、血小板5-HT、ADP-P2Y12反应蛋白(PRU值)低于焦虑组,差异有统计学意义(t=-5.261,-3.064,-3.738,-3.062,-2.845;P0.01),抑郁症和非抑郁组上述指标比较,差异有统计学意义(t=-6.312,-4.868,-4.603,-3.675,-3.386;P0.01)。结论 :AMI合并焦虑或抑郁能促使血小板活化,增加血小板聚集率,可能弱化氯吡格雷疗效。     

高功率多普勒血流探测仪结合血流成像仪观察氯吡格雷对高血压大鼠微循环的影响

目的:观察抗血小板药物氯吡格雷对高血压大鼠微循环的影响。方法:SPF级雄性13周龄自发性高血压大鼠(SHR),随机分为溶剂对照组和氯吡格雷组,每组5只,分别灌胃1ml 0.5%羧甲基纤维素钠(CMC-Na)和氯吡格雷溶液(10mg/kg),每日一次。连续四周后,用高功率激光多普勒血流探测仪(LDF)检测大鼠脑皮质、耳廓及趾血流量、血细胞聚集度和血流速度,用血流成像仪(LDPI)观察脑血流分布状态。统计学分析检测指标的组间差异。结果:除血细胞聚集度和脑皮质血流速度外,氯吡格雷组大鼠上述LDF检测指标值均高于溶剂对照组(P0.05或P0.01),LDPI检测脑皮质血流分布曲线整体右移,脑皮质高血流量(800-1500PU)面积百分比较溶剂对照组明显增加(P0.01)。结论:氯吡格雷可明显改善SHR微循环障碍。     

急性冠脉综合征患者介入术后可视化血液流变性与血小板功能的相关性分析

 目的:应用可视化血液流变性检测仪（MC-FAN）并结合血小板功能指标的检测,观察急性冠脉综合征(ACS)介入术后患者血液流变性的变化特点,并探讨患者血液流变性可视化结果与血小板功能指标的相关性。方法:纳入74例ACS介入术后1～3年的患者,21例健康者为健康对照组,应用MC-FAN检测2组人群的血液通过模拟人体毛细血管的时间（MC-FAN TT）和比较不同时段的结果,同时检测血小板聚集性、血小板黏附性、血小板P-选择素、血小板衍生生长因子BB和血管假性血友病因子指标,观察ACS介入术后患者的MC-FAN 结果与血小板功能的相关性。结果:与健康对照组相比,ACS介入术后患者的血流MC-FAN TT延长(P<0.01),红细胞变形能力减弱,白细胞附壁及血小板的黏附、聚集相对增多;ACS介入术后患者的血小板最大聚集率、血小板黏附率、血小板P-选择素水平及血小板衍生生长因子BB水平均高于健康对照组（P<0.01）;2组间血管假性血友病因子差异无统计学意义（P>0.05）。组内相关性分析显示：MC-FAN TT与血小板功能存在相关性,其中10 μL MC-FAN TT和30 μL MC-FAN TT与P-选择素呈正相关（r=0.601,P<0.01;r=0.334,P<0.01）;60 μL MC-FAN TT与血小板最大聚集率呈正相关（r=0.527,P<0.01）;100 μL MC-FAN TT与血小板黏附率呈正相关（r=0.815,P<005）。结论:ACS介入术后患者的可视化血液流变性及血小板功能异常,MC-FAN TT与血小板功能存在相关性,MC-FAN检测仪可客观地评价介入术后患者血液流动的状态。     

替格瑞洛与氯吡格雷对急性心肌梗死冠脉介入术后血小板聚集的影响

目的:研究替格瑞洛与氯吡格雷对急性心肌梗死冠脉介入术后血小板聚集的影响。方法:将2017年5月至2018年5月本院收治的急性心肌梗死冠脉介入治疗患者102例依随机数表法分为对照组和观察组,每组51例。对照组患者采用氯吡格雷(75 mg·次-1,1次·d-1,口服治疗,连续治疗12 M)治疗,观察组给予替格瑞洛(90mg·次-1,2次·d-1,口服治疗,连续治疗12 M)治疗。治疗前与治疗12 M后分别使用无创血液动力学检测仪检测每搏输出量（Stroke volume,SV）、左心室射血分数（Left ventricular ejection fraction,LVEF）、左心室舒张末期内径（Leftventricularenddiastolicdiameter,LVEDD）、左心室收缩末期容积（Leftventricularend systolic volume,LVESV）,并测定患者血小板聚集率,同时记录并对比两组患者在治疗12 M过程中主要心血管不良事件（Major adverse Cardiovascular events,MACE）及药物不良反应发生情况。结果:与治疗前相比,两组的SV、LVEF水平均明显增加（P<0.05）,其中观察组更为显著（P<0.05）;各治疗组的LVEDD、LVESV水平均明显降低（P<0.05）,其中观察组更为显著（P<0.05）;与治疗前相比,各治疗组的血小板聚集率均明显降低（P<0.05）,其中观察组更为显著（P<0.05）;观察组MACE事件发生率与不良反应总发生率均低于对照组（P<0.05）。结论:冠脉介入术后对急性心肌梗死患者使用替格瑞洛治疗,可达更好的心功能改善效果,对血小板聚集抑制作用更显著,且术后MACE事件及药物不良反应发生率均较低,具有较高临床推荐价值。     

支架置入非ST段抬高急性冠脉综合征患者血小板功能及替罗非班的干预

背景:目前,经皮冠状动脉介入围手术期如何给予个体化的抗血小板治疗国内外尚没有达成共识;在抗血小板的联合用药、用药时机和应用时间方面也存在着较多的争议。目的:观察非ST段抬高急性冠脉综合征患者支架置入前后血小板活性的变化及替罗非班的干预作用。方法:125例患者随机分为2组:替罗非班组(n=62):阿司匹林+氯吡格雷+替罗非班;对照组(n=63):阿司匹林+氯吡格雷;两组均行经皮冠状动脉介入治疗,观察支架置入前及置入后6,24h及7d,经花生四烯酸诱导的血小板最大聚集率、血小板活化标志物CD62p变化;两组患者经皮冠状动脉介入治疗后30d临床事件及出血事件的发生率。结果与结论:支架置入后6h,对照组血小板最大聚集率及CD62p水平较置入前显著升高(P0.01);替罗非班组则显著低于置入前及对照组(P0.01);置入后24h,两组之间及与置入前相比,血小板最大聚集率及CD62p差异无显著性意义(P0.05);置入后7d,替罗非班组血小板最大聚集率较置入前降低(P0.05)。替罗非班组经皮冠状动脉介入治疗后30d临床缺血事件的发生率低于对照组(P0.05);两组患者出血事件发生率差异无显著性意义(P0.05)。提示支架置入后6h,非ST段抬高急性冠脉综合征患者血小板功能被进一步激活。在双重抗血小板(阿司匹林+氯吡格雷)治疗的基础上,替罗非班对接受支架置入非ST段抬高急性冠脉综合征患者的血小板功能有进一步的抑制作用。     

氯吡格雷常见不良反应与抗血小板药物的相互作用

<正>氯吡格雷是一种新型噻吩吡啶类衍生物,其抗血小板机制是:它的活性代谢产物可选择性不可逆地与血小板表面二磷酸腺苷(ADP)受体P2Y12结合,减少ADP结合位点,阻断ADP对腺苷环化酶的抑制作用,抑制纤维蛋白原与血小板糖蛋白GPIIb/IIIa受体结合及继发的ADP介导的糖蛋白GPIIb/IIIa复合物的活化,进而抑制血小板聚集。     

肝硬化的血小板功能异常的探讨

检测了64例肝硬化患者的血小板计数,血块退缩试验,血小板粘附试验,血小板聚集试验,血小板因子皿活性,结果发现:29例(45.3%)血小板计数减少.另外35 例血小板计数正常患者中,10例(28.4%)血小板粘附试验降低,25例(71.4%)血小板聚集试验降低.19例(54.4%)血小板因子Ⅲ活性减弱,这变化与肝功能损害的程度有关.在肝功能Child分级中,A、B、C级各组间血小板功能的异常有显著差异(x~2=10.1164,P<0.01),提示肝硬化患者存在血小板功能异常,血小板功能检查也可作为检测肝功能损害程度的辅助指标.     

氯吡格雷抵抗对急性心肌梗死合并糖尿病患者冠脉介入治疗预后的影响

目的：观察急性心肌梗死合并糖尿病且接受直接经皮冠脉介入治疗的患者氯吡格雷抵抗发生的情况及其对远期预后的影响。方法：连续入选2011年1月1日~2012年12月31日在我院接受直接经皮冠脉介入治疗,出院后随访>1年的急性心肌梗死合并糖尿病患者119例,所有患者均在服用氯吡格雷负荷量24 h后进行血栓弹力图检测,根据ADP诱导的血小板抑制率分为对照组(ADP抑制率≥50%,82例)和观察组(即氯吡格雷抵抗组,ADP抑制率<50%,37例)。记录患者的临床特点、生化指标、随访期间死亡和主要不良心血管事件(main adverse cardiac events,MACE)发生情况。结果：临床随访平均(783±241) d,氯吡格雷抵抗的发生率为31%。随访1年内总的MACE发生率为7.6%。氯吡格雷抵抗组1年内的MACE发生率明显高于对照组(16.2% vs.3.7%,P=0.025)。氯吡格雷抵抗和长期(1年以上)MACE发生无关(P=0.334);多因素Cox回归分析,氯吡格雷抵抗对患者的长期死亡率无明显影响。结论：接受直接经皮冠状动脉介入治疗的糖尿病合并急性心肌梗死患者存在明显的氯吡格雷抵抗现象。氯吡格雷抵抗会增加这些患者介入术后1年内发生主要心脏不良事件的风险,而对其1年以上的长期预后无显著影响。     

血小板和巨大血小板的检测研究

目的 :研究不同方法计数血小板总数和检测巨大血小板的差异。方法 :12 0例血样同时采用Advia 12 0仪器法、STKS仪器法和手工方法进行血小板总数检查 ,并将 12 0例标本逐一制成血涂片、瑞氏染色和显微镜镜检。结果 :3种方法对血小板总数的检测没有明显差异 (P >0 .0 5 )。但 3种方法对巨大血小板的检出率有明显不同 ,Advia 12 0法 4 1.6 7% (5 0 / 12 0 ) ,STKS法 2 9.17% (35 / 12 0 ) ,手工法镜检 32 .5 0 % (39/ 12 0 ) ,二仪器法之间以及Advia 12 0法与手工法镜检之间差异有显著性意义 (P <0 .0 5 )。结论 :采用仪器法和手工法检查血小板总数 ,其结果没有差异 ;虽然 3种方法都可检测巨大血小板 ,但以Advia 12 0法检出率较高 ,准确性较好。     

Platelet gels

Platelet gels (PG) are blood-derived biomaterials that are generally obtained through the activation of a platelet-rich plasma or a platelet concentrate by thrombin or calcium chloride, resulting in the simultaneous conversion of fibrinogen into a fibrin gel and in the generation of a platelet releasate rich in a physiological cocktail of growth factors. To reinforce the physical strength of the fibrin network, a fibrinogen-rich fraction – generally cryoprecipitate – can be added to the platelet fraction prior to activation, resulting in the generation of platelet fibrin glue (PFG). PG and PFG, prepared from single donations, either autologous or allogeneic, are increasingly used, alone or in combination with grafting materials, in various field of regenerative medicine where the presence of growth factors is expected to stimulate the healing of soft or hard tissues. Being obtained from human blood, they are physiological and biodegradable preparations and do not induce tissue necrosis. So far, the viral safety of most allogeneic PG and PFG relies on donors selection and donation testing, as is the case for all non-virally inactivated blood components for transfusion. Major fields of clinical applications of PG and PFG in osseous tissue regeneration include maxillo-facial surgery, implantology, reconstructive and plastic surgery. Platelet gels are also used for enhancing the healing of soft tissues, most particularly recalcitrant lower extremity ulcers of various aetiologies, and burns. Newer promising indications include the treatment of osteo-arthritis and joint inflammation, and the repair of musculoskeletal tissue lesions in sports medicine. Autologous PG and PFG are mostly ‘home-made’ single-donor preparations prepared using medical devices. They suffer from the variability in donor characteristics and in isolation procedures of the platelet fraction. Clinical application methods are not standardized. Variability in autologous product characteristics is high, and optimal content of growth factors is unknown, confusing the analysis of product efficacy. The evidence of clinical benefits of these products based on controlled clinical studies is lacking in most indications, although many case studies do support an objective benefit in soft and probably hard tissues healing. Improvement in the standardization and formulation of PG and PFG is a mandatory step forward for improving the reliability and the predictability of clinical outcomes of these interesting blood preparations.     

Platelet fibrinogen

Platelet fibrinogen has been studied in normal, thrombasthenic, and hypofibrinogenaemic subjects. It has been differentiated into adsorbed (plasma) and extractable (intraplatelet) fractions. Isotopic studies suggest that exchange does not occur between intraplatelet and plasma fibrinogen and it appears possible that the intra-platelet fraction may be derived from the megakaryocyte. Six of nine thrombasthenic patients were found to have a severe deficiency of both adsorbed and extractable fibrinogen. Since the remaining three had near-normal platelet fibrinogen and all nine failed to aggregate it is improbable that the failure to adsorb fibrinogen is responsible for the defect in aggregation. Magnesium partially corrects adhesion to fibrin and clot retraction by these platelets, but has not been found to influence their fibrinogen adsorption. It is considered that the basic platelet surface defect, of varying severity, is responsible for the abnormalities of adsorption, aggregation, and adhesion in thrombasthenia. In the case of congenital hypofibrinogenaemia, fibrinogen transfusion corrects the long bleeding time, platelet-adsorbed fibrinogen, and the ability of platelets to spread on glass. It is possible that fibrinogen influences the surface properties of human platelets, although the final mechanism is not determined.     

富血小板血浆中血小板浓度对血小板聚集的影响

目的探讨富血小板血浆（PRP）血小板浓度对血小板聚集的影响。方法随机收集107名门诊体检健康志愿者静脉血浆,分离PRP和PPP（贫血小板血浆）后,用血液分析仪测定PRP血小板浓度,按PRP浓度用自身PPP配成50×109/L～400×109/L浓度梯度的血浆,用血浆比浊法测血小板聚集率。结果 PRP血小板浓度在50×109/L～400×109/L,二磷酸腺苷（ADP）和花生四烯酸（AA）诱导的血小板聚集率分别为（10.4±8.7）%至（55.3±9.9）%和0%至（75.2±10.1）%,血小板聚集率随血小板浓度的增高而增高,血小板浓度为250×109/L时,聚集率增幅减缓,血小板浓度小于150×109/L时,血小板聚集率明显降低。结论 PRP血小板浓度对血小板聚集的影响明显,血小板聚集试验PRP血小板浓度大于150×109/L;血浆比浊法血小板聚集试验适宜的血小板浓度为250×109/L。     

Gray Platelet Syndrome

Seven hepatoblastomas were studied by electron microscopy, and four of these were studied by immunohistochemistry. Five tumors were purely epithelial, and two were mixed epithelialmesenchymal. They showed a spectrum of cellular differentiation ranging from primitive epithelial cells to differentiated cells resembling adult hepatocytes. Glycogen, lipid, basal lamina, and canaliculi were present in all cases. Mitochondria with large, membrane-bound, amorphous inclusions were present in one tumor, and large, complex, basal cell processes were present in two tumors. Ultrastructural features most characteristic of hepatocytes were most common in fetal type hepatoblastomas. Immunoreactive chromogranin cells were present in two tumors, one of which also contained immunoreactive somatostatin cells. The somatostatin-positive tumor had cells with granules resembling those seen in somatostatin-containing cells of normal pancreas and somatostatin-containing neuroendocrine carcinomas. Other immunoreactive substances were present, including α₁-antitrypsin (four cases), vimentin (embryonal cells in four cases; fetal cells in three cases), low-molecular weight cytokeratin (embryonal cells in three cases; fetal cells in four cases), and high-molecular weight cytokeratin (embryonal cells in one case; fetal cells in two cases). Osteoidlike material was positive for epithelial membrane antigen, vimentin, and S-100 protein.