急性脑血管病外周血血小板表面P-选择素阳性表达率变化及药物干预

目的　探讨血小板活化因子P 选择素 (CD62P)在急性脑血管病患者中的改变及其用奥扎格雷钠治疗后的变化。方法　采用流式细胞仪测定 78例急性脑梗死患者及 2 5例健康对照组外周血血小板表面P 选择素阳性表达率 ,将病例组分为奥扎格雷钠组与非奥扎格雷钠组 ,治疗前后测P 选择素作对比观察。 30例急性脑出血患者入院后测外周血P 选择素并与健康对照组作对比。结果　急性脑梗死患者外周血血小板表面P 选择素阳性表达率显著高于对照组 (P <0 .0 0 1 ) ;用奥扎格雷钠治疗后的外周血血小板表面P 选择素阳性表达率明显低于非奥扎格雷钠组(P <0 .0 1 ) ;奥扎格雷钠组治疗后较治疗前血小板活化因子P 选择素阳性表达率明显降低 (P <0 .0 5) ;急性脑出血患者外周血血小板表面P 选择素阳性表达率明显高于健康对照组 (P <0 .0 0 1 ) ;合并冠心病、高血压、糖尿病的脑梗死患者与单纯脑梗死患者外周血P 选择素阳性表达率无明显差异(P >0 .0 5)。结论　血小板活化在急性出血及脑梗死的发生、发展中起重要作用。     

奥扎格雷钠对急性脑梗死患者血浆溶血磷脂酸水平的影响

目的观察奥扎格雷钠对急性脑梗死患者血浆溶血磷脂酸(LPA)水平的影响。方法65例急性脑梗死患者随机分为奥扎格雷钠组(35例)和常规治疗组(30例),两组均给予阿司匹林、长春西汀注射液;奥扎格雷钠组加用奥扎格雷钠治疗1个疗程。结果奥扎格雷钠组和常规治疗组治疗前血浆LPA水平显著高于正常对照组(P0.01),治疗后血浆LPA水平逐渐降低。奥扎格雷钠组治疗后10d血浆LPA水平显著低于常规治疗组(P0.01)。结论奥扎格雷钠能显著降低急性脑梗死患者的血浆LPA水平,抑制血小板聚集。     

不同抗血小板药物联合治疗进展性脑梗死的比较

目的比较不同抗血小板药物(阿司匹林、氯吡格雷和奥扎格雷)联合治疗对进展性脑梗死患者的血小板活化水平和神经功能的影响。方法将97例急性进展性脑梗死患者随机分为A组(阿司匹林+氯吡格雷)、B组(阿司匹林+奥扎格雷)、C组(氯吡格雷+奥扎格雷),分别比较各组患者在治疗前、治疗3天后和治疗14天后血小板CD62P表达水平和临床神经功能缺损程度评分。结果三组患者联合抗血小板治疗14天后,与同组治疗前相比,血小板CD62P的表达水平和神经功能缺损程度评分均有明显下降(P<0.05),其中A组(阿司匹林+氯吡格雷)和C组(氯吡格雷+奥扎格雷)较B组(阿司匹林+奥扎格雷)下降更明显,差异有统计学意义(P<0.05)。结论对于进展性脑梗死患者尽早联合使用两种抗血小板药物治疗,可以取得较好的疗效,其中阿司匹林联合氯吡格雷和氯吡格雷联合奥扎格雷方案治疗效果更好。     

奥扎格雷钠治疗急性脑梗死的疗效观察

目的观察奥扎格雷钠治疗急性脑梗死的疗效。方法将90例急性脑梗死患者随机分为治疗组和对照组，各45例。两组均常规应用尼莫地平、丹参注射液等。治疗组应用奥扎格雷钠；对照组应用阿司匹林。比较两组疗效。结果治疗组总有效率为91．1％；对照组为71．1％，两组比较差异有显著性（P〈0．05）。结论奥扎格雷钠较阿司匹林治疗急性脑梗死有较好的疗效。     

奥扎格雷对急性脑梗死患者血浆溶血磷脂酸(LPA)水平的影响

目的探讨急性脑梗死患者血浆溶血磷脂酸（LPA）水平变化，奥扎格雷对急性脑梗死患者血浆LPA水平的影响。方法84例急性脑梗死患者，随机分为2组：奥扎格雷组（44例）、阿斯匹林组（40例），奥扎格雷组给予奥扎格雷静点，阿斯匹林组给予阿斯匹林口服。两组在发病24h、1w及2w时定测定血浆LPA含量。年龄相匹配的75名健康体检者作为对照组，测定血浆LPA含量。结果脑梗死患者血浆LPA水平明显高于对照组。奥扎格雷组血浆LPA水平下降较阿斯匹林组更明显，差异有显著性（P（0．01）。结论急性脑梗死患者血浆LPA水平明显升高，奥扎格雷可降低急性脑梗死血浆LPA水平，效果优于阿斯匹林。     

奥扎格雷钠联合灯盏花素治疗老年短暂性脑缺血发作的疗效

目的探讨奥扎格雷钠联合灯盏花素治疗老年短暂性脑缺血发作的临床疗效。方法选取该院于2010年1月至2014年9月收治的180例老年短暂性脑缺血发作患者,随机分为两组,各90例。对照组给予常规治疗,加用奥扎格雷钠治疗。观察组给予常规治疗,加用奥扎格雷钠联合灯盏花素治疗。结果观察组总有效率高于对照组(P0.01)。治疗后,观察组患者高切黏度、全血低切黏度、血浆黏度、纤维蛋白原小于对照组(P0.01)。治疗后,观察组患者血小板活化因子(PAF)、血浆2颗粒膜蛋白(GMP-140)少于对照组(P0.01)。治疗后,观察组患者短暂性脑缺血发作发作停止时间小于对照组(P0.01)。结论奥扎格雷钠联合灯盏花素治疗老年短暂性脑缺血发作疗效显著,可有效改善患者的各项生化指标,阻止短暂性脑缺血发作向脑梗死转变,有利于患者的预后。     

奥扎格雷钠与东菱迪芙联合治疗进展型脑梗死的临床研究

目的临床观察奥扎格雷钠与东菱迪芙联合治疗进展型脑梗死的疗效。方法将108例进展型脑梗死患者随机分为治疗组和对照组各54例，治疗组为奥扎格雷钠联合东菱迪芙治疗，对照组为奥扎格雷钠治疗，两组均辅以常规治疗。结果治疗组总有效率（92．5％）优于对照组（79．6％），P〈0．05，两组均无严重出血倾向。结论奥扎格雷钠与东菱迪芙联合治疗进展型脑梗死的疗效优于对照组。     

低分子肝素钙与奥扎格雷钠联合治疗急性脑梗死疗效观察

目的探讨低分子肝素钙、奥扎格雷钠联合治疗急性脑梗死的临床疗效。方法将2003年8月～2005年4月黑龙江一重集团公司医院120例急性脑梗死住院患者随机分为治疗组（60例）和对照组（60例）。治疗组应用低分子肝素钙与奥扎格雷钠，对照组常规治疗，均在发病6～48h内给药。治疗后进行神经功能缺损评分并评价临床疗效。结果神经功能缺损改善，治疗组明显优于对照组（P〈0．01）。临床疗效评价总有效率治疗组95％，对照组75％，治疗组明显优于对照组（P〈0．05）；显效率治疗组75％，对照组43．3％，治疗组明显优于对照组（P〈0．01）。结论低分子肝素与奥扎格雷钠联合治疗急性脑梗死能有效中止病情进展，改善神经功能缺损，临床疗效好，安全性高。     

奥扎格雷钠治疗进展性脑梗死的临床观察

目的观察奥扎格雷钠治疗进展性脑梗死的临床疗效。方法将80例进展性脑梗死病人随机分为两组。对照组采用常规治疗,治疗组在常规治疗基础上加用奥扎格雷钠80mg加入生理盐水500mL中静脉输注,连用14d。结果两组治疗后神经功能缺损评分均较治疗前明显下降(P<0.05或P<0.01),但以治疗组下降显著,且治疗组临床疗效优于对照组(P<0.05)。结论奥扎格雷钠治疗进展性脑梗死优于常规治疗。     

奥扎格雷钠对脑梗死患者血液流变学的影响

血小板聚集在脑梗死的发病中发挥着重要的作用。血小板是血栓的主要组成成分 ,它又可通过其活化后释放的血栓烷 A2 (TXA2 )等花生四烯酸产物促进血液凝固 ,有利于血栓形成。奥扎格雷钠为血栓烷A2 (TXA2 )合成酶的抑制剂 ,能选择性抑制 TXA2 合成酶 ,同时也能增强前列环素 I2 (PGI2 )合成酶 ,具有抗血小板聚集、扩张血管、增加血流量和供氧量作用 ,达到治疗和消除血栓的功效。本文观察了奥扎格雷钠治疗脑梗死时患者血液流变学的变化。1　资料与方法1 .1　病例选择　 70例脑梗死患者均经 CT或 MRI证实。随机分为两组 :1奥扎格雷钠组 :…     

重组组织型纤溶酶原激活剂静脉溶栓治疗急性脑梗死的临床研究

目的:探讨重组组织型纤溶酶原激活剂(rt-PA)静脉溶栓治疗急性脑梗死(ACI)患者的疗效及安全性。方法:将发病在4.5 h内ACI患者139例,且均符合静脉溶栓适应证,按入院顺序分为rt-PA组(61例)和对照组(ACI)(78例),分别给予rt-PA静脉溶栓和奥扎格雷钠治疗。采用NIHSS及mRS评分比较2组患者治疗后24 h、7 d、90 d的疗效及安全性。结果:rt-PA组治疗后7 d,NIHSS评分较对照组改善更显著。rt-PA组90 d mRS评分优于对照组。2组病死率、症状性颅内出血发生率无统计学差异。结论:ACI患者4.5 h内给予rt-PA静脉溶栓,疗效优于奥扎格雷钠,且较为安全。     

奥扎格雷钠联合依达拉奉治疗急性脑梗死140例疗效评价

目的探讨奥扎格雷钠联合依达拉奉治疗急性脑梗死的临床疗效及安全性。方法将急性脑梗死患者140例随机分为联合组和对照组各40例。对照组行常规治疗：口服阿司匹林,静滴奥扎格雷钠、胞二磷胆碱等;联合组在对照组用药基础上同时给予依达拉奉静滴。两组疗程均为14 d。治疗前、治疗后第3天、第7天、第14天对两组患者进行神经功能缺损（NIHSS）评定、临床疗效评价和日常生活能力（Barthel指数,BI）评分,并监测凝血常规、肝肾功能、血脂、血糖和心电图。结果联合组临床疗效优于对照组;两组患者治疗后NIHSS评分和BI评分均有明显改善;治疗后第3天、第7天和第14天联合组的改善程度均优于对照组,差异均有统计学意义（P〈0.05）。结论奥扎格雷钠联合依达拉奉治疗急性脑梗死临床效果显著、安全,能明显改善患者的神经功能缺损。     

奥扎格雷在急性冠脉综合征中抗血小板作用的研究

目的：通过对血小板活化指标血小板颗粒膜糖蛋白（CD62p）及血小板脂膜蛋白（CD61）与血浆假性血友病因子（vWF）的观测,探讨抗血小板药物奥扎格雷（Ozagrel）对急性冠脉综合征（ACS）患者血小板功能的影响。方法：应用流式细胞术（FCM）和酶联免疫吸附试验（ELISA）测定60例ACS患者应用奥扎格雷治疗前后静脉血CD62p,CD61和血浆vWF的表达水平,对两者在ACS时的水平进行对比分析。同时设20例健康体检者做对照组。结果：CD62p值：ACS患者的为（85.02±7.22）%,明显高于对照组（32.56±6.39）%（P〈0.05）,药物治疗后ACS组下降至（65.20±8.17）%（P〈0.05）,其水平变化与vWF、心绞痛和缺血ST-T改善一致;CD61表达量为（89.38±7.13）%,与正常组比较差异无显著性（P〉0.05）,药物干预治疗前、后比较,差异亦无显著性（P〉0.05）。结论：CD62p是血小板活化的敏感指标,且与vWF和临床症状改变一致。推测急性冠脉综合症患者应用奥扎格雷有进一步增强抗血小板的作用。     

奥扎格雷加灯盏细辛治疗不稳定型心绞痛

目的观察奥扎格雷加灯盏细辛治疗不稳定型心绞痛疗效。方法选择不稳定型心绞痛病人60例，实验组除常规治疗外给予奥扎格雷加灯盏细辛，对照组则加用复方丹参注射液。观察治疗前后临床、心电图、血小板电泳率及血液流变学变化。结果实验组可明显缓解心绞痛及心电图缺血改变，治疗后血小板电泳率显著增快，血液流变学指标改善。结论奥扎格雷加灯盏细辛能有效治疗不稳定型心绞痛。     

老年急性冠状动脉综合征患者血小板P选择素、血管性血友病因子的变化及氯吡格雷干预的临床研究

目的观察老年急性冠状动脉综合征(ACS)患者血小板P选择素和血管性血友病因子(vWF)的变化,及抗血小板聚集药物氯吡格雷干预后的临床相关研究,探讨它们在ACS发病机制中的作用和相互联系。方法选取60例老年ACS患者,其中急性心肌梗死(AMI)患者30例,不稳定型心绞痛(UAP)患者30例,另设对照组30例。随机将UAP分为常规治疗组和氯吡格雷(75mg/d)组,AMI组应用抗血小板聚集药物(氯吡格雷300mg+阿司匹林)联合治疗,采用全血法流式细胞术及血浆酶联免疫吸附法测定各组治疗前后血小板P选择素、vWF水平变化,同时探讨P选择素与vWF的相关关系。结果老年ACS患者P选择素、vWF水平[AMI组P选择素(9.74±1.97)%,vWF(272.24±28.62)%;UAP组P选择素(8.87±1.78)%,vWF(215.81±22.01)%]显著高于正常对照组[P选择素(2.27±1.30)%,vWF(112.45±13.22)%](P<0.001)。常规治疗组和氯吡格雷组均可降低UAP患者P选择素与vWF水平[常规治疗组P选择素治疗前(8.60±1.39)%,治疗后(5.60±2.18)%,降低(2.97±1.82)%,vWF治疗前(217.52±25.68)%,治疗后(170.17±20.88)%,降低(47.34±24.31)%;氯吡格雷组P选择素治疗前(9.15±2.11)%,治疗后(4.24±1.73)%,降低(4.89±2.02)%,vWF治疗前(214.10±18.35)%,治疗后(151.72±12.66)%,降低(62.38±21.58)%],但氯吡格雷组较常规治疗组降低的程度更明显(P<0.05),AMI组联合治疗后P选择素与vWF水平均低于治疗前[P选择素(2.27±1.30)%,vWF(112.45±13.22)%](P<0.001),但仍高于对照组(P<0.001)。老年ACS患者P选择素水平与vWF水平成正相关(r=0.365,P<0.05)。结论P选择素、vWF与ACS的发病过程有关,可能是老年ACS不稳定斑块的识别和预测指标。     

Platelet P-selectin expression in patients with sickle cell disease who undergo apheresis

Activated platelets have been identified in patients with sickle cell disease. However, the association of platelet P-selectin expression and automated red cell exchange procedures in these patients is not well known. We hypothesized that altered whole platelet P-selectin expression is associated with automated red cell exchange. Flow cytometric quantification of platelet P-selectin expression was carried out in 23 patients with sickle cell disease before and after automated red cell exchange. P-selectin expression was quantified as a binding index for platelet P-selectin (the percentage of positive platelets multiplied by the mean fluorescence of positive platelets). The patients were divided into two groups: individuals with painful vaso-occlusive crises (four women and five men; group 1) and those in a steady state (six women and eight men; group 2). The 33 exchange procedures were evaluated prospectively and used acid-citrate-dextrose A solution (whole blood to anticoagulant ratio = 14:1). Platelet P-selectin expression did not significantly change after automated red cell exchange. Clinical factors such as the volume of replacement fluid and the citrate infusion rate did not correlate with postapheresis platelet P-selectin expression. In addition, the association of platelet P-selectin expression and automated red cell exchange was independent of other laboratory factors (hematocrit level, hemoglobin S level, platelet count, and nitric oxide level). Finally, the difference between the study groups regarding platelet P-selectin expression before and after apheresis was insignificant. In conclusion, automated red cell exchange procedures do not induce platelet P-selectin expression in patients with sickle cell disease in the steady state or in vaso-occlusive crisis.     

Aspirin inhibits surface glycoprotein IIb/IIIa, P-selectin, CD63, and CD107a receptor expression on human platelets.

Platelet inhibition after aspirin therapy reduces the risk for the development of acute coronary syndromes. However, the mechanism by which aspirin affect platelets other than by prostaglandin blockade is unclear. We sought to determine the in vitro effects of aspirin on the surface expression of nine platelet receptors using whole blood flow cytometry. Blood from 24 healthy volunteers was incubated for 30 min with 1.8 and 7.2 mg/l phosphate-buffered saline-diluted acetylsalicylic acid in the presence or absence of apyrase. Platelet serotonin release, and the surface expression of platelet receptors with or without apyrase were determined using the following monoclonal antibodies: anit-CD41 [glycoprotein (GP)IIb/IIIa], CD42b (GPIb), CD62p (P-selectin), CD51/CD61 (vitronectin receptor), CD31 [platelet/endothelial cellular adhesion molecule-1 (PECAM-1)], CD107a [lysosomal associated membrane protein (LAMP)-1], CD107b (LAMP-2), CD63 (LIMP or LAMP-3), and CD151 (PETA-3). Samples were then immediately fixed with 2% paraformaldehyde, and run on the flow cytometer within 48 h. Aspirin does not affect serotonin release from human platelets. Dose-dependent inhibition of GPIIb/IIIa, P-selectin, CD63, and CD107a receptor expression was observed in the aspirin-treated whole-blood samples. Apyrase potentiates the effects of aspirin, and independently inhibits PECAM-1. In addition to the known effect of irreversibly inhibiting platelet cyclooxygenase-1, thereby blocking thromboxane A(2) synthesis, it appears that aspirin exhibits direct effects on selective major platelet receptors.     

Regulation of adhesion molecule expression by human synovial microvascular endothelial cells in vitro

Objective. To examine the in vitro expression of E-selectin, P-selectin, intercellular adhesion molecule 1 (ICAM-1), ICAM-2, vascular cell adhesion molecule 1 (VCAM-1), and platelet–endothelial cell adhesion molecule 1 (PECAM-1) by synovial microvascular endothelial cells (SMEC) in comparison with microvascular neonatal foreskin endothelial cells (FSE) and macrovascular human umbilical vein endothelial cells (HUVE). Methods. Cultured endothelial cells were treated for 4 hours with medium alone or tumor necrosis factor α (TNF α). The expression of endothelial adhesion molecules was evaluated by flow cytometry, cell enzyme-linked immunosorbent assay, and Northern blot analysis. Results. SMEC continuously expressed E-selectin under basal culture conditions, whereas FSE and HUVE did not. TNF α treatment of rheumatoid arthritis (RA) SMEC resulted in sustained peak expression of E-selectin for up to 24 hours, which subsequently declined but remained elevated even at 72 hours. In contrast, peak E-selectin expression in FSE and HUVE occurred between 4 hours and 16 hours after TNF α treatment and then declined to near basal levels by 24–48 hours. SMEC expressed significantly higher levels of ICAM-1 compared with HUVE under basal culture conditions. There was no difference between SMEC, FSE, and HUVE in the expression of P-selectin, VCAM-1, ICAM-2, or PECAM-1. Northern blot analysis demonstrated that the levels of E-selectin expression by TNF α-stimulated endothelial cells correlated with their respective messenger RNA levels. Conclusion. Regulation of E-selectin and ICAM-1 expression in RA synovial endothelium is different from that in neonatal foreskin and human umbilical vein endothelium. The augmented expression of adhesion molecules in RA synovial endothelium may facilitate the recruitment of leukocytes to this site.     

奥扎格雷联合阿司匹林对急性脑梗死高血小板聚集率的干预研究

目的观察奥扎格雷对急性脑梗死的临床疗效和实验室指标的变化。方法将血小板聚集率增高的急性脑梗死患者随机分成两组,治疗组108例患者给予奥扎格雷80mg＋5%葡萄糖250m l静脉滴注,2次/d,同时服阿司匹林100 mg,1次/d;对照组110例,给阿司匹林100mg,1次/d。结果治疗组和对照组患者治疗后血小板聚集率都降低,而治疗组比对照组降低更明显,Scand inavian卒中评分两组治疗后比治疗前均提高,治疗组（9.90分）比对照组（6.86分）更明显。差异有显著性意义（P〈0.01）。治疗组与对照组治疗前、后凝血酶时间和纤维蛋白原水平比较差异无显著性意义（P〉0.05）。结论奥扎格雷和阿司匹林治疗急性脑梗死近期临床疗效是肯定的,而奥扎格雷疗效更显著,使血小板聚集率降低更明显。     

Soluble PECAM-1, but not P-selectin, nor osteonectin identify acute myocardial infarction in patients presenting with chest pain.

We sought to determine plasma levels of platelet/endothelial cell adhesion molecule-1 (PECAM-1), P-selectin, and platelet-derived osteonectin, and prospectively compare these data with the discharge diagnosis in patients presenting with chest pain in a community hospital Emergency Department. Soluble antigens were measured by ELISA in 44 subjects including patients with acute myocardial infarction (AMI) (n = 13), chest pain of noncardiac origin (n = 17), and compared to those of age- and sex-matched healthy controls (n = 14). Elevated soluble PECAM-1 (64.5 +/- 18.3 ng/ml, p = 0.019), but not P-selectin (149.5 +/- 49.8 ng/ml, p = NS), nor osteonectin (549. 5 +/- 159.1 ng/ml, p = NS), occurred in the AMI group as compared to patients with noncardiac chest pain (46.2 +/- 7.5 ng/ml, 118.2 +/- 40.1 ng/ml, and 619.4 +/- 74.4 ng/ml, respectively). Increased plasma PECAM-1 may serve as a useful marker in the early detection of patients with AMI. Larger studies will be necessary to confirm the utility of soluble PECAM-1 in identifying AMI among patients presenting with chest pain.