糖尿病对缺血性卒中患者阿司匹林抵抗的影响

目的：研究糖尿病对缺血性卒中患者发生阿司匹林抵抗的影响。方法将100例均经头部CT或MRI证实为缺血性卒中的患者,随机分为糖尿病组和非糖尿病组；各组患者均服用阿司匹林100 mg/d,疗程≥7 d。用二磷酸腺苷(ADP)和花生四烯酸(AA)作为诱导剂测定血小板聚集功能,根据血小板聚集试验结果来观察各组阿司匹林抵抗的发生率。结果糖尿病组阿司匹林抵抗的发生率与非糖尿病组阿司匹林抵抗的发生率有显著性差异(<0.05)。结论糖尿病患者更易发生阿司匹林抵抗。     

小剂量阿司匹林对急性脑梗死患者花生四烯酸代谢

花生四烯酸代谢产物血栓素A2(TXA2)和前列腺素I2(PGI2)以及血小板在体内血栓形成中起重要作用. 本文观察了急性脑梗死(ACI)患者服用阿司匹林前后血栓素B2、6-酮前列环素及血小板聚集率的变化, 旨在探讨阿司匹林对ACI患者血栓素A2、前列腺素I2及血小板聚集的影响, 为急性脑梗死临床治疗提供理论依据.     

脑梗死急性期患者血小板膜糖蛋白Ia C807T基因多态性和血小板功能

目的:探讨血小板膜糖蛋白(GP)Ia C807T基因多态性及与脑梗死急性期患者血小板功能的关系。方法:应用聚合酶链反应限制性片段长度多态性(PCR-RELP)方法检测97例急性期脑梗死患者(脑梗死组)及99例正常对照者(对照组)的GPIa C807T基因型,采用全血流式细胞术检测血小板P选择素(CD62P)表达率,采用比浊法检测花生四烯酸、二磷酸腺苷诱导的血小板最大聚集率(MARAA、MARADP)。结果:脑梗死组GPIa T等位基因频率高于对照组,差异有统计学意义(χ2=5.369,P<0.05);脑梗死组CD62P表达率、血小板MARAA、MARADP高于对照组(P<0.05)。对照组TT+CT基因型CD62P表达率和MARADP高于CC基因型(P<0.05);脑梗死组TT+CT基因型CD62P表达率和MARAA、MARADP与CC基因型差异无统计学意义(P>0.05)。结论:GPIaC807T可能是脑梗死发病的遗传危险因素。血小板活化和聚集功能增强可能是T等位基因促进脑梗死发病的机制之一。     

2型糖尿病患者血小板聚集功能与肾微血管病变的关系

目的 :探讨 2型糖尿病 (DiabetesMellitus,DM )患者血小板聚集活性与肾微血管病变的关系。方法 :测定 15 6例 2型DM患者血小板功能指标 ,如血小板聚集率、血小板平均体积和肾微血管功能指标 ,如 2 4h尿白蛋白 (Alb)、2 4h尿β2 微球蛋白 ( β2 Microglobulin ,β2 MG)排泄量 ,分析二类指标的相关性。结果 :随着DM患者病情进展 ,尿A1b和尿β2 MG排泄不断增加 ,血小板聚集率逐渐上升 ,血小板平均体积逐渐增大 ,两者成明显正相关。结论 :血小板功能活性升高可能是糖尿病肾脏微血管损伤的促进因素之一 ,抑制血小板过度活化 ,是糖尿病治疗中的重要环节     

麝香保心丸对稳定性心绞痛患者血小板聚集的影响

<正>目的:观察麝香保心丸对稳定性冠心病患者血小板聚集的影响。方法:选取90例稳定性心绞痛患者,随机分为口服阿司匹林组和口服麝香保心丸加阿司匹林组(n均=45)。测定患者服药前及服药1个月后血小板聚集率及血小板活化因子水平变化。结果:用药前阿司匹林组血小板聚集率为(47.54±12.56)%,血小板活化因子水平为(40.86±11.74)nmol/L,麝香保心丸加阿司匹林组血小板聚集率为(48.98±12.71)%,血小板活化因子水平为(41.33±12.09)nmol/L,两组间无统计学差异;用药后阿司匹林组血小板聚集率为(35.47±9.08)%,     

新型血小板功能分析仪PL-11监测血小板聚集功能的应用价值

目的 评价连续血小板计数法血小板功能检测仪PL-11监测血小板功能的价值.方法 分别应用SC-2000光学比浊法(LTA)与PL-11连续血小板计数法两种血小板功能检测仪,检测30例急性心肌梗死急诊入院患者,入院时、负荷剂量(600mg)服用氯吡格雷后的第8小时、PCI术后第三天晨起时的血小板聚集功能,分析两种仪器检测结果的相关性及PL-11在氯吡格雷抵抗(clopidogrel resistance,CR)的诊断准确性.结果 在测试人群中,LTA测得最大血小板聚集率(MAR)范围均较PL-11广;所有受试者在刚入院未服用氯吡格雷时,PL-11与LTA不相关(相关系数r=0.35,P=0.058＞0.05),在术前氯吡格雷大剂量冲击后及术后第三天两次检测的MAR存在相关性(r=0.500和0.571,P＜0.01);两种仪器三次检测结果均为第一次和第三次明显高于第二次,差异具有统计学意义(P ＜0.05);PL-11用于诊断CR的ROC曲线下面积为0.798(95％ CI:0.621～0.964).结论 PL-11连续血小板计数法与“金标准”的(LTA)浊法检测血小板聚集功能具有一定的相关性,其检测结果可供临床及实验室参考.     

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。     

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。     

银蒺胶囊对心绞痛(血瘀证)患者血液流变性的影响

目的了解银杏叶和白蒺藜提取物的复合制剂银蒺胶囊(JL-GE)对冠心病心绞痛(血瘀证)患者血液流变性的影响。方法43例心绞痛(血瘀证)患者随机分为JL-GE治疗组和阿斯匹林对照组,分别服用JL-GE45mg,3次/日和阿斯匹林75mg,1次/日,治疗时间1月。检测患者治疗前后的血液流变性和血小板聚集率指标。结果治疗1月后,治疗组患者血小板一分钟聚集率AGG(1)由(57.44±5.78)%降至(48.45±4.54)%(P<0.01),血小板最大聚集率AGG(M)由(77.66±8.05)%降至(65.56±5.69)%(P<0.01)。与对照组相比,治疗组AGG(1)和AGG(M)的降低幅度均无显著差异(P>0.05);治疗组低切变率下全血黏度由(11.69±2.02)mPa·s降至(9.40±1.04)mPa·s(P<0.01),高切变率下全血黏度和血浆黏度均降低,但没有统计学意义(P>0.05)。结论JL-GE可以降低冠心病心绞痛(血瘀证)患者低切变率下全血黏度和血小板聚集率,改善血液流变性。     

中性粒细胞对洗涤血小板聚集功能的影响

目的:观察非激活或激活的中性粒细胞(PMN)对洗涤血小板聚集功能的影响。方法:采用Born方法测定血小板聚集功能。结果:非激活的PMN(5×10⁹cells/L)上清液对ADP和花生四烯酸(AA)诱导的血小板聚集具有显著抑制作用,阿司匹林可增强这种抑制作用;肉豆寇佛波醇(fMLP)及血小板活化因子(PAF)激活的PMN悬液或其上清液均能活化血小板聚集,且PMN悬液的诱聚作用比其上清液更强;阿司匹林对fMLP或PAF激活的PMN悬液或其上清液均无明显抑制作用。结论:不同状态(非激活或激活状态)的PMN对正常血小板的反应性表现出完全相反的作用,即非激活的PMN抑制血小板反应性,而激活的PMN则具有促血小板活化聚集作用。     

急性脑梗塞患者血浆内皮素与血小板内钙含量和聚集关系的探讨

本文用放射免疫分析测定了１６例急性脑梗塞病人的血浆内皮素，用比浊法测定了血小板聚集，用Ｆｕｒａ－２／ＡＭ荧光技术测定了血小板内游离Ｃａ＾２＋含量。急性脑梗塞病人血浆内皮素明显升高（Ｐ〈０．０１），血小板聚集率增设增高（Ｐ〈０．０１），血小板内Ｃａ２＾＋含量增高（Ｐ〈０．０１），且观察到ＡＤＰ诱导的血小板聚集与血小板内Ｃａ＾２＋含量之间呈正相关（ｒ＝０．７８，Ｐ〈０．０１），而血浆内皮素与血小反聚集     

Aspirin non-responsiveness in Korean subjects on dual anti-platelet treatment determined by two different platelet function assays

Several techniques are available for measuring platelet function during aspirin therapy, but none is well standardized, and the reported incidence of aspirin non-responders varies widely, from 5 to 50%. We evaluated the optical platelet aggregation test and the Platelet Function Analyzer-100 test (PFA-100) for assessing aspirin responsiveness in patients receiving dual anti-platelet therapy, and we measured the incidence of non-responders to aspirin among Koreans. The study enrolled 88 participants including 51 patients on dual anti-platelet therapy, 31 controls, and 6 other volunteers. Optical platelet aggregation in response to 4 agonists and aggregation using the PFA-100 test were determined. In addition, medical records, including the results of platelet aggregation tests, were reviewed for 351 patients receiving aspirin therapy. The results showed good correlation between the PFA-100 test using a collagen/epinephrine cartridge (CEPI) and the optical platelet aggregation test using each agonist. The platelet aggregation test using arachidonic acid revealed marked suppression of aggregation (>98% inhibition) in patients taking aspirin; this value was highly correlated with the PFA-100 results using the CEPI cartridge. Seven of 351 Korean subjects (2.0%) receiving aspirin treatment were non-responsive to aspirin. This study shows that the optical platelet aggregation test using arachidonic acid gave an accurate assessment of the response to aspirin, and that results of the PFA-100 test using the CEPI cartridge correlated well with results of the optical platelet aggregation test.     

急性心肌梗塞患者血小板聚集性改变及药物的影响

急性心肌梗塞患者肾上腺素诱导血小板聚集性降低,与病情有一定关系,一般两周内恢复;5-羟色胺诱导聚集阳性率及不解聚率均明显高于正常对照组;每日口服100mg阿斯匹林明显抑制5-羟色胺及肾上腺素诱导聚集,但不能完全抑制尿激酶引起的血小板聚集增加;蝮蛇抗栓酶对5-羟色胺诱导聚集有明显抑制作用。     

血小板功能变化在血栓性疾病中的诊断意义

分别检测５种血栓性疾病（高血压、心绞痛、急性心肌梗塞、脑梗塞和糖尿病）的血小板粘附、血小板聚集、血栓素Ｂ２（ＴＸＢ２）、６－酮－前列腺素Ｆ１α（６－ｋｅｔｏ－ＰＧＦ１α）以及全血、血浆粘度等指标。结果显示：上述５种疾病的血小板功能均有不同程度和类型变化。所有检测项目中变化最明显的是β－ＴＧ和血小板粘附性,其次为ＰＦ４和ＴＸＢ２,再次为血小板聚集性和６－ｋｅｔｏ－ＰＧＦ１α。这一发现有助于医师评估上述试验价值以及根据实验条件选择敏感试验。     

Platelet function during thrombolytic therapy with anistreplase

Platelets are likely to play a role during thrombolytic therapy of acute myocardial infarction, but their exact involvement is not fully understood at present. The effects of thrombolytic agents on platelet function have mainly been studied using in vitro experiments and results are rather controversial; data from in vivo studies are rare. We studied 10 patients with acute myocardial infarction, who were treated with intravenous anistreplase. Use of aspirin or other anti-platelet drugs were not allowed. Before and after thrombolysis, blood was collected for determining ex vivo platelet aggregation and platelet factor 4, β-thromboglobulin and thromboxane-B₂ in plasma. Immediately after anistreplase, the aggregation of platelets was significantly inhibited: aggregation induced by ADP decreased to 67±36% (mean±SD) of pretreatment (P<0.05), by arachidonic acid to 29±29% (P<0.005) and by collagen to 58±46% (P<0.05). The aggregation defect was transient; after 6–12h aggregation had returned to normal. Then, a significant stimulation of ADP-induced aggregation became apparent, lasting until 24–48h after thrombolysis; possibly this was mediated by heparin. The platelet proteins and thromboxane-B₂ were significantly elevated before thrombolysis and showed a steady decrease after anistreplase. In the first phase of anistreplase therapy, we found no indications of platelet activation. Additional in vitro studies confirmed these findings. Antibodies to streptokinase did not affect platelet function in these patients.     

Use of native or platelet count adjusted platelet rich plasma for platelet aggregation measurements

BACKGROUND: It is still not clear whether native or platelet count adjusted platelet rich plasma (PRP) should be used for platelet aggregation measurements.AIM: To evaluate the necessity of using adjusted PRP in platelet function testing. METHODS: Platelet aggregation with native PRP and adjusted PRP (platelet count: 250/nl, obtained by diluting native PRP with platelet poor plasma) was performed on the Behring Coagulation Timer (BCT(R)) using ADP, collagen, and arachidonic acid as agonists. Healthy subjects, patients on antiplatelet treatment, and patients with thrombocytosis (platelet counts in PRP > 1250/nl) were investigated. RESULTS: No significant differences in the maximum aggregation response were seen when using either native or adjusted PRP from healthy subjects and patients on antiplatelet treatment. Nevertheless, some patients taking aspirin or clopidogrel showed reduced inhibition of ADP and arachidonic acid induced aggregation in adjusted PRP but not in native PRP. The maximum velocity of healthy subjects and patients on antiplatelet treatment varied significantly as a result of the degree of dilution of the adjusted PRP. Surprisingly, the BCT provided good results when measuring platelet aggregation of native PRP from patients with thrombocytosis, whereas commonly used aggregometers could not analyse platelet aggregation of native PRP in these patients. CONCLUSION: The time consuming process of PRP adjustment may not be necessary for platelet aggregation measurements. Moreover, using adjusted PRP for monitoring aspirin or clopidogrel treatment may falsify results. Therefore, it may be better to use native PRP for platelet aggregation measurements, even in patients with thrombocytosis.     

噻氯匹啶对老年常见血栓性疾病患者血小板聚集性及血液流变学的影响

对42名老年常见血栓性疾病非急性梗塞期患者随机给予噻氯匹啶(ticlopidine,TP)125～250 mg/日或阿斯匹林(aspirin,ASA)162.5mg/日,疗程36～39日。服药前后分别测定三项血小板(platelct,Pt)聚集指标,TP组尚同步作血液流变学及血液粘弹性测定。结果发现:对于二磷酸腺苷(ADP)诱导的Pt聚集,TP有极显著的抑制作用(P<0.01),且TP之抑制作用超过ASA(P<0.05)。TP能明显延长出血时间(BT)(P<0.05)、对多项血液流变学及血液粘弹性指标无影响、也无明显副作用。作者认为TP防治血栓性疾病可能是通过降低Pt聚集率和延长BT而起作用的。     

Effects of aspirin and clopidogrel versus oral anticoagulation on platelet function and on coagulation in patients with nonvalvular atrial fibrillation (CLAFIB)

The aim of the study was to evaluate the effect of two antithrombotic therapies on platelet function and on coagulation in patients with nonvalvular atrial fibrillation (NVAF). Twenty patients with NVAF were treated with aspirin (300 mg/day) and clopidogrel (75 mg/day) for 2 weeks immediately followed by oral anticoagulation (target international normalized ratio 2.0-3.0). Parameters of platelet function and coagulation were evaluated before antithrombotic therapy, at the end of aspirin plus clopidogrel and during subsequent anticoagulation treatment. Aspirin plus clopidogrel significantly inhibited platelet aggregation, fibrinogen receptor activation and release of P-selectin and prolonged in vitro bleeding time (p < 0.01). Coagulation parameters (platelet-dependent thrombin generation, antithrombin III, thrombin-antithrombin III complex, prothrombin fragment 1 + 2) were not significantly affected. During the subsequent oral anticoagulation phase platelet function was not substantially reduced; however, coagulation parameters were significantly inhibited (p < 0.001). The results indicate that combined antiplatelet therapy is superior to aspirin monotherapy in inhibiting platelet function but does not seem to substantially modulate coagulation cascade in patients with NVAF.     

Platelet aggregation in patients taking anticoagulants after valvular surgery: evaluation by a laser light-scattering method

 The effects of anticoagulants in the early phase of platelet aggregation in patients with an artificial cardiac prosthesis are unclear. Newly developed particle-counting methods that employ light scattering (LS) can be used to quantify changes in the number of platelet aggregates of different sizes after administration of an aggregating stimulus. Using an LS method, we studied the effects of warfarin and aspirin on aggregation in patients with an artificial cardiac prosthesis. Forty-seven patients undergoing valvular surgery were divided into two groups: 25 patients were treated with warfarin alone (group 1), and 22 patients were treated with both warfarin and aspirin (81 mg/day) (group 2). The international normalized ratio (INR) value was controlled at 2.0–2.5 in both groups. Blood samples were obtained before surgery to obtain control values and on days 21 through 27 after surgery. Platelet aggregation was evaluated after administration of 2.0 μg/ml collagen: small (9–25 μm), medium (25–50 μm), and large (50–70 μm) aggregates were counted. Particle counting by the LS method showed no inhibition of platelet aggregation in group 1 (warfarin alone). The conventional optical density (OD) method yielded a similar result. In group 2 (warfarin plus aspirin), the LS method showed that generation of large aggregates after stimulation was significantly decreased versus presurgery (P = 0.046), whereas the quantity of small aggregates was increased (P = 0.003). The OD methods showed aggregation to be significantly decreased in this group (P < 0.001). Our findings suggest that warfarin does not appear to suppress platelet aggregation. Although aspirin appears to suppress platelet function, it does not affect the initial phase of aggregation. Platelet dysfunction caused by aspirin is due mainly to inhibition of the development of small aggregates into larger aggregates. Received: January 7, 2002 / Accepted: May 30, 2002 Correspondence to:K. Kawahito