急性脑梗死患者血小板-白细胞聚集体的变化

目的探讨急性脑梗死患者血小板-白细胞聚集体(PLA)的变化,及其与血浆C反应蛋白(CRP)、血小板聚集率(PAgT)的关系。方法对46例脑梗死患者(脑梗死组)和24例年龄、性别相配的非脑血管病患者(对照组)进行PLA、CRP和PAgT的检测。结果脑梗死组血小板-单核细胞聚集体(PMA)、PAgT和CRP分别为(13.00±0.76)%、(59.46±3.07)%和(9.39±1.28)mg/L,对照组分别为(6.55±0.29)%、(39.38±5.42)%和(2.37±0.46)mg/L,两组间差异有极显著性(均P<0.01);脑梗死组PLA、血小板-中性粒细胞聚集体(PNA)和血小板-淋巴细胞聚集体(PLyA)高于对照组,但两组间差异无显著性。脑梗死组PMA与CRP和PAgT呈极显著正相关(r=0.390、0.500,均P<0.01)。结论脑梗死急性期患者的炎症反应和血小板活化水平显著增高。     

急性脑梗死患者血小板-白细胞聚集体的动态变化及意义

目的探讨急性脑梗死患者血小板-白细胞聚集体(platelet-leukocyte aggregation,PLA)的动态变化及其临床意义。方法收集作者医院就诊的158例急性脑梗死患者以及30名健康体检者(对照组)为研究对象,根据瘫痪肢体肌力或神经功能评分量表(NIHSS)评分变化将脑梗死患者分为进展性脑梗死组和无进展脑梗死组,采用流式细胞技术检测健康对照组以及脑梗死患者不同时期的PLA水平。结果进展性脑梗死组血小板-单核细胞聚集体(platelet-monocyte aggregations,PMA)水平在进展期明显升高,而后逐渐下降(P<0.05),无进展脑梗死组PMA水平逐渐下降,差异有统计学意义(P<0.05);进展性和无进展脑梗死组PLA、血小板-淋巴细胞聚集体(platelet-lymphocyte aggregations,PLyA)、血小板-中性粒细胞聚集体(platelet-neutrophilic aggrega-tions,PNA)水平无明显动态变化(P>0.05);PMA水平与NIHSS评分呈正相关(r=0.12,P<0.05)。结论 PLA不仅在脑梗死的发病中发挥作用,而且可反映急性脑梗死患者病情的严重程度。     

血小板-白细胞聚集体在进展性脑梗死中的作用

目的 探讨血小板-白细胞聚集体(platelet-leukocyte aggregation,PLA)在进展性脑梗死发病中的作用.方法 检测158例急性脑梗死患者血压、血糖、血脂、C反应蛋白(CRP)、纤维蛋白原、PLA,并分析进展性脑梗死发生的危险因素.结果 158例脑梗死中,37例发展为进展性脑梗死.进展性脑梗死组入院次日血小板-单核细胞聚集体( platelet-monocyte aggregations,PMA)高于无进展性脑梗死组(P＜0.05),而PLA、血小板-淋巴细胞聚集体(platelet-lymphocyte aggregations,PLyA)、血小板-中性粒细胞聚集体(platelet-neutrophilic aggregations,PNA)在两组间的比较无统计学意义(P＞0.05);PMA水平与血糖、血胆固醇、CRP、纤维蛋白原、收缩压呈正相关;收缩压(OR0.11,95％ CI 0.05 ～0.28,P=0.00)、PMA( OR 5.65,95％ CI 2.47 ～ 12.96,P=0.00)为进展性脑梗死发生的独立危险因素.结论 血小板-白细胞聚集体在进展性脑梗死的发病过程中发挥重要作用.     

参芎葡萄糖注射液对脑梗死患者血肿瘤坏死因子α的影响

目的观察参芎葡萄糖注射液对于脑梗死患者血肿瘤坏死因子α(tumor necrosis factorα,TNF-α)的影响和临床治疗效果。方法 88例脑梗死患者随机分为2组,A组40例,进行常规性血小板聚集治疗;B组48例,在常规治疗的基础上加用参芎葡萄糖注射液,连续应用21d,观察2组患者治疗前和治疗21d后的血TNF-α水平和美国国立卫生研究院卒中量表(National Institute of Health Stroke scale,NIHSS)评分。结果 2组治疗前血TNF-α水平和NIHSS评分无明显差异,治疗21d后血TNF-α水平和NIHSS评分均有不同程度降低,B组减低较A组更明显,差异均有统计学意义(P0.05)。结论参芎葡萄糖注射液能够提高脑梗死患者的神经功能,可能与其降低血TNF-α水平有关。     

超早期去骨瓣减压术对大面积脑梗死老年患者神经功能及血小板活化能力水平的影响

目的探讨超早期去骨瓣减压术对大面积脑梗死老年患者神经功能及血小板活化能力水平的影响。方法将郑州中康医院2018年6月至2019年6月收治的123例大面积脑梗死老年患者按照手术时间分组,对照组61例发病24~48 h内行去骨瓣减压术,观察组62例超早期(发病24 h内)行去骨瓣减压术。观察两组患者的疗效、神经功能、血小板活化能力水平及手术并发症。结果观察组疗效优于对照组(P<0.05);观察组术后1个月、6个月末用美国国立卫生研究院卒中量表(NIHSS)评分较对照组低(P<0.05);观察组术后1周末血小板淋巴细胞聚集体(PlyA)、血小板-单核细胞聚集体(PMA)、血小板-白细胞聚集体(PLA)及血小板中性粒细胞聚集体(PNA)的百分比水平较对照组低(P<0.05);观察组手术并发症发生率(6%)较对照组(20%)低(P<0.05)。结论超早期去骨瓣减压术可降低大面积脑梗死老年患者血小板活化水平,改善神经功能,提高治疗效果并减少手术并发症。     

双重抗血小板治疗对急性脑梗死患者血小板活化及聚集的影响

目的 观察急性脑梗死患者血小板CD62p表达及血小板聚集的变化,并探讨双重抗血小板治疗对其的影响.方法 将60例急性脑梗死患者随机分为阿司匹林治疗组(A组)和阿司匹林+银杏达莫注射液治疗组(B组),每组各30例.采用流式细胞技术,于发病次日及治疗2周后对血小板CD62p的表达进行检测,并观察2组患者治疗前后Scandinavian卒中量表(SNSS)评分、血小板聚集率(PAR)的变化.结果 与治疗前比较,2组治疗后PAR(ADP) 、PAR(AA)、 CD62p均显著降低,差异有统计学意义(P＜0.01);2组治疗后SNSS评分均高于治疗前,差异有统计学意义(P＜0.05);2组治疗后比较,B组PAR(ADP)、 CD62p低于A组,差异有统计学意义(P＜0.01).结论 与单用阿司匹林相比,阿司匹林联用银杏达莫注射液具有更强的抑制血小板活化及聚集的作用.     

P-选择素基因S290N和P-选择素糖蛋白配体-1基因M62I多态性与缺血性脑梗死血小板白细胞聚集体的相关性探讨

目的探讨血小板白细胞聚集体在缺血性脑梗死中的变化以及与P-选择素基因S290N和P-选择素糖蛋白配体-1基因M62I多态性的关系。方法选取58例缺血性脑梗死患者作为病例组,20例正常人群作为对照组。病例组分为大动脉粥样硬化性脑梗死(LAA)19例,小动脉闭塞性脑梗死(SAO)39例。运用流式细胞技术检测所有受试者的血小板白细胞聚集体(PLA)、血小板单核细胞聚集体(PMA)、血小板淋巴细胞聚集体(PLy A)和血小板中性粒细胞聚集体(PNA)水平。并运用基因测序方法检测P-选择素基因S290N和P-选择素糖蛋白配体-1基因M62I多态性。结果 PMA%在病例组与对照组、LAA与对照组、SAO与对照组间差异有统计学意义(P=0.000,P=0.018,P=0.000)。PNA%在病例组与对照组、LAA与对照组间差异有统计学意义(P=0.045,P=0.002)。PNA%在LAA组SELP基因S290N位点SS和SN基因型间差异有统计学意义(P=0.008)。PLA%在LAA组PSGL-1基因M62I位点MM、MI和Ⅱ基因型间差异有统计学意义(P=0.046)。结论 PMA和PNA与缺血性脑梗死发病有关,SELP基因S290N位点SN基因型以及PSGL-1基因M62I位点MM基因型会增加LAA发生风险。     

吲哚美辛对脑梗死急性期炎症反应的影响

目的研究吲哚美辛对急性脑梗死(ACI)患者血清C反应蛋白(CRP)及可溶性细胞间粘附分子-1(sICAM-1)水平的影响,探讨吲哚美辛对脑梗死急性期炎症反应的影响。方法将60例ACI患者随机分为吲哚美辛治疗组和常规治疗组,并选取正常体检者30人组成对照组。在治疗前及治疗第7天、第14天检测血清CRP和sICAM-1含量,并进行神经功能缺损程度评分(NIHSS)评定。结果两组治疗前血清sICAM-1、CRP含量较对照组显著升高(P0.01),治疗后较治疗前显著下降(P0.01),且吲哚美辛治疗组较常规治疗组下降显著(P0.05);两组治疗14d时NIHSS较治疗前显著下降(均P0.01),且吲哚美辛治疗组较常规治疗组下降明显(P0.05);吲哚美辛治疗组未出现明显副反应,耐受性良好。结论吲哚美辛能明显降低ACI患者血清CRP及sICAM-1水平;有助于ACI患者的神经功能恢复并且安全性较好。     

阿司匹林抵抗与血小板活化在脑梗死复发中的作用

目的探究阿司匹林抵抗与血小板活化在脑梗死复发中的重要作用。方法选取2012-06-2014-06我院收治的165例脑梗死患者为研究对象,其中55例复发脑梗死患者设为A组,110例初发脑梗死患者设为B组,选取同期50例健康体检者设为C组。统计3组阿司匹林抵抗率、血小板聚集率和PLA(血小板白细胞聚集体)水平,并进行对比分析。结果A组PLA水平和血小板聚集率明显高于B、C 2组,且C组最低,差异有统计学意义(P0.05);A组阿司匹林抵抗率为27.3%,与B组的11.8%相比较,差异有统计学意义(P0.05)。结论脑梗死复发过程中血小板活化和阿司匹林抵抗均起到重要作用,需尽早发现阿司匹林抵抗,调整脑梗死患者的二级预防策略,以保证治疗的有效率。     

奥扎格雷对急性脑梗死患者血小板CD62p和CD63表达的影响及其疗效

目的观察奥扎格雷对急性脑梗死(ACI)患者血小板CD62p、CD63表达的影响及其疗效。方法将64例ACI患者随机分为奥扎格雷治疗组和血塞通治疗组(对照组),采用流式细胞术检测ACI患者治疗前后及正常人(正常组)血小板CD62p、CD63的表达;观察奥扎格雷治疗组和对照组的临床疗效并进行比较。结果ACI患者血小板CD62p、CD63表达水平明显高于正常组(均P<0.01);奥扎格雷治疗组与对照组治疗后血小板CD62p、CD63表达水平较治疗前均有明显下降(P<0.05～0.01),奥扎格雷治疗组又明显低于对照组,差异有显著性(均P<0.05)。奥扎格雷治疗组的基本痊愈率、显著进步率、总有效率明显高于对照组(均P<0.05)。结论ACI发病后血小板CD62p、CD63表达水平显著增高;奥扎格雷有明显抑制血小板表达CD62p、CD63的作用,对ACI的治疗效果显著。     

急性脑梗死患者单核细胞-血小板聚集水平检测及临床意义

目的观察急性脑梗死患者外周血单核细胞与血小板聚合物CD14~+、CD42a~+水平,了解脑梗死患者单核细胞-血小板聚集情况及临床价值。方法用流式细胞术检测急性脑梗死组80例和对照组60例外周血单核细胞CD14~+、血小板膜糖蛋白CD42a~+双阳性细胞所占的百分比,并对脑梗死患者进行NIHSS评分。结果脑梗死组外周血单核细胞与血小板聚合物CD14~+、CD42a~+阳性率(25.46±8.91)高于对照组(14.25±6.36)(P0.05);且脑梗死时不同NIHSS评分组间单核细胞与血小板聚合物CD14~+、CD42a~+阳性率比较:轻型组20.24±9.66、中型组25.35±8.41、重型组32.40±8.85三组间比较P0.05,与病情严重程度明显相关。结论急性脑梗死早期单核细胞与血小板聚合物CD14~+、CD42a~+表达明显增高,检测单核细胞与血小板聚合物CD14+、CD42a+水平对于脑梗死患者早期诊断及预测病情轻重具有重要的临床应用价值。     

血细胞参数、血清蛋白水平与急性脑梗死的相关性研究

目的 探讨红细胞分布宽度(RDW)、平均血小板体积(MPV)和血清白蛋白(ALB)、球蛋白(GLB)水平与急性脑梗死的关系。方法 通过比较148例急性脑梗死患者与148例体检健康者的血红细胞、血小板参数和血清蛋白水平,探讨其与急性脑梗死的关系。结果 急性脑梗死组RDW、MPV、血小板分布宽度(PDW)、GLB水平明显高于对照组(P<0.01),ALB水平、白蛋白/球蛋白比率(A/B)明显低于对照组(P<0.01),logistic回归分析显示RDW、MPV、GLB的升高和ALB的降低与急性脑梗死独立相关。结论 RDW、MPV、GLB的升高和ALB水平的降低可能是急性脑梗死的独立危险因素。     

Aspirin treatment does not attenuate platelet or leukocyte activation as monitored by whole blood flow cytometry

Despite undoubtful clinical evidence of anti-platelet effects of aspirin, previous studies demonstrate little inhibition by aspirin treatment of single platelet activation as measured by flow cytometry. This discrepancy was further evaluated using flow cytometric measurements of circulating platelet-leukocyte aggregates (PLAs), which may be a more sensitive marker of platelet activation in vivo than measurements of activation markers on single platelets. Blood samples were obtained from 15 healthy subjects before and after aspirin treatment (75 and 500 mg daily for 1 week). Platelet (P-selectin expression) and leukocyte (CD11b expression) activation and platelet-leukocyte aggregation were monitored by whole blood flow cytometry. Approximately 1% platelets in unstimulated samples were P-selectin-positive, i.e., circulating activated platelets, and about 3% of leukocytes were circulating as PLAs; neither of these parameters were reduced by aspirin treatment. Circulating platelet micro-aggregates were not influenced by aspirin either. In vitro stimulation with ADP, thrombin, or PAF increased platelet P-selectin expression and thus PLA formation, but these responses were not affected by aspirin. Leukocyte CD11b expression, a marker of leukocyte secretion, was not significantly influenced by aspirin either in unstimulated samples or upon in vitro stimulation. Thus, the present data support the concept that thromboxane generation is of little importance for the activation of single platelets; the platelet inhibiting effect of aspirin is seen mainly in the presence of close cell-cell contact, which enhances the importance of thromboxane. Multiple mechanisms may contribute to the remarkable clinical anti-thrombotic effect of aspirin.     

Increased platelet aggregability during exercise in patients with previous myocardial infarction. Lack of inhibition by aspirin

The aim of the present study was to investigate the effects of acute exercise on platelet aggregability, blood coagulation, and fibrinolysis in patients with recent myocardial infarction, and to examine these effects in relation to two different antithrombotic regimens. Forty patients (mean age 60 years) were investigated 3 months after a myocardial infarction. They were randomized to antithrombotic treatment with either warfarin (INR 2.8-4.2) or aspirin 160 mg daily. They performed a standardized ergometer bicycle exercise test. Blood was drawn before and after the exercise. The platelet function tests included a platelet aggregate ratio (PAR), which, in the presence of aggregates, is<1. The coagulation products remained largely unchanged during the exercise, whereas the fibrinolytic activity and the catecholamine levels increased significantly. At baseline, PAR was lower in the warfarin group than in the aspirin group. During exercise, PAR was significantly reduced in both study groups (0.75 vs. 0.80), indicating increased platelet aggregability. Beta-thromboglobulin decreased in both groups. The increased platelet aggregability after exercise despite aspirin is probably due to activation by catecholamines. This implies that aspirin may have a limited antithrombotic effect during physical exercise and probably also in other situations with increased catecholamine levels.     

藻酸双酯钠对急性脑梗死患者血小板α颗粒膜蛋白的影响

目的研究藻酸双酯钠对急性脑梗死患者血小板a颗粒膜蛋白的影响及临床疗效。方法将急性脑梗死患者随机分藻酸双酯钠(PSS)、阿司匹林(ASA)与噻氯匹定(TP)3个治疗组,测量治疗前及治疗后3d、7d、14d的血小板α颗粒膜蛋白-140含量,并观察治疗前后临床神经功能状况。结果3组治疗后3d、7d、14d血浆GMP-140水平较治疗前明显降低,PSS组患者的神经功能恢复优于ASA与TP组。结论PSS具有抗血小板聚集作用,能有效改善急性脑梗死患者神经功能缺损症状,提高其日常生活能力。     

Prophylaxis of thromboembolic disease and platelet-related changes following total hip replacement: a comparative study of aspirin and heparin-dihydroergotamine

A prospective study involving 120 consecutive patients undergoing total hip replacement was performed to compare the effectiveness of aspirin (high and low dose) or a combination of heparin plus dihydroergotamine (heparin-DHE) in preventing isotopic and phlebographic deep vein thrombosis (DVT), and to evaluate their effect on postoperative platelet changes. Phlebographic DVT was demonstrated in 9 cases (30%) in control group, in 1 (3.3%) in aspirin (high-dose) group (p less than 0.01), in 1 (3.3%) in aspirin (low-dose) group (p less than 0.01) and in 5 (16.6%) in heparin-DHE group (p = NS). Aspirin was able to reduce the postoperative increase in circulating platelet aggregates, platelet factor 4 and beta-thromboglobulin observed in control group. This study shows that aspirin is effective in the prevention of DVT for patients undergoing total hip replacement. Small aspirin dose (250 mg/day) represents an effective form of prophylaxis in these patients.     

PAS三联疗法对急性脑梗死患者血脂、血清sCD40L及MMP-9水平及颈动脉易损斑块稳定性的影响

目的 探讨普罗布考、阿司匹林、他汀类药物(PAS)三联疗法对急性脑梗死患者血脂、血清超敏C-反应蛋白(hs-CRP)、可溶性CD40配体(sCD40L)及基质金属蛋白酶-9(MMP-9)水平的影响,观察其对颈动脉易损斑块稳定性的影响.方法 根据颈动脉超声检查结果分为颈动脉稳定斑块组(n=45)和颈动脉易损斑块组(n=90).将稳定斑块组作为对照组,按随机数字法将易损斑块组分为AS组(n=45,阿司匹林100mg/d,阿托伐他汀20mg/d,口服)和PAS组(n=45,AS基础上加用普罗布考片,0.25/次,2次/日,口服).比较治疗前后血脂、血清hs-CRP、sCD40L和MMP-9水平;观察治疗前后颈动脉内-中膜厚度(IMT值)、斑块Crous积分及斑块回声变化.结果 治疗后4w,两组中TG、TC、LDL-C、血清hs-CRP、sCD40L和MMP-9水平均下降,PAS组中各项指标下降幅度均大于AS组,差异具有显著性(P均＜0.01);治疗后12个月,两组IMT值和斑块Crous积分较治疗前减少,且PAS组两项指标低于AS组,PAS组低回声斑块回声增强例数高于AS组(P均＜0.01).结论 PAS三联疗法是一种安全有效的治疗方法,具有更强的降脂抗炎作用,可逆转和稳定斑块.     

Increased platelet aggregates in patients with transient ischemic attacks.

In order to evaluate the pathogenetic importance of platelet aggregates in cerebrovascular disease, a platelet count ratio method was used to study 66 patients with transient ischemic attacks (TIAs). Thirty normal subjects and 22 patients without thromboembolic disorders were also included as controls. The mean platelet aggregate ratio of the TIA group was 0.75 +/- 0.03 SEM which was significantly lower than that of normal subjects (0.90 +/- 0.02) or patients controls (0.88 +/- 0.01) (P less than 0.01). Seventeen patients with TIA were then treated with aspirin (1,200 mg) and dipyridamole (200 mg) daily. The platelet aggregate ratios were normalized in 13 patients. Of four patients who did not respond to this regimen, one did respond to sulfinpyrazone. When sulfinpyrazone was discontinued, recurrence of symptoms was preceded by an increase in platelet aggregates. These findings suggest that platelet aggregates may play an important role in the pathogenesis of cerebrovascular insufficiency. The determination of platelet aggregates appears useful in selecting patients for antiplatelet therapy.     

Pathogenesis of early thrombus formation in experimental vein graft

When inferior vena cava of rabbit was replaced by 3 cm long woven Tetron (polyethylene terephthalates) graft under bolus injection of heparin (50 U/kg), the graft was completely occluded at 1.5 +/- 0.35 h after the bolus injection of heparin. In order to elucidate the pathogenesis of this early thrombus formation, the same venous grafting was performed in rabbits receiving anticoagulants and/or anti-platelet agents and the thrombus formation was analyzed by scanning electron microscopy as well as by measuring the weight of dehydrated thrombus. The grafts in rabbits receiving an additional bolus heparin were patent until the anticoagulant effect disappeared and the thrombus formed in these grafts was composed of platelet aggregates anchored to synthetic fibers and of erythrocytes trapped into fibrin network. The patency of the graft was maintained at least 5 hours in rabbits receiving intravenous injection of aspirin (20 mg/kg) or oral administration of ticlopidine (100 mg/kg/day x 5 days prior to the grafting). The weight of dehydrated thrombus of the graft in aspirin and ticlopidine treated rabbits was 25 +/- 5 and 12 +/- 4 mg respectively, which were significantly lower than that of control group (59 +/- 9 mg). Ultrastructural studies revealed in these grafts piles of erythrocytes with fibrin network which were layered over the synthetic fibers without bridges of platelet aggregates. Also, the treatment with anti-platelet agents, especially ticlopidine, resulted in inhibition of organization of fibrin network. These observations indicate that thrombus in venous graft is formed by anchorage of platelet aggregates to synthetic fibers followed by activation of coagulation to form network of polymerized fibrin entrapping erythrocytes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Collagen-Induced Platelet Aggregates,Diabetes, and Aspirin Therapy Predict Clinical Outcomes in Acute Ischemic Stroke

Background: Aggregation of platelets is a trigger for additional development of larger thrombi. This study aimed to identify factors that may affect platelet aggregability and their role in clinical outcomes in acute ischemic stroke. Methods: Consecutive acute ischemic stroke patients (n = 352) who were transferred within 24 hours after its onset were enrolled. Peripheral venous blood was sampled to measure platelet aggregability and other parameters. Results: Mean values of spontaneous small-sized platelet aggregates and collagen- or adenosine diphosphate (ADP)-induced large-sized aggregates were elevated in acute ischemic stroke. In atherothrombotic stroke (n = 178), collagen and ADP-induced large-sized aggregates were positively correlated with HbA1c, respectively. High incidence of the modified Rankin Scales (mRS) 5-6 at discharge was associated with diabetes complication (odds ratio [OR] 8.77, 95% confidence interval [CI] 1.32-57.56). The proportion of patients who were functionally independent (the mRS 0-2) at discharge was lower in the middle tertile of collagen and ADP-induced large-sized aggregates than their low tertile (OR 2.46, 95% CI 1.09-5.58; OR 2.43, 95% CI 1.05-5.59, respectively). Prestroke administration of aspirin recovered the proportion of independence at discharge (OR 0.25, 95% CI 0.06-0.99), and ameliorated incidence of the mRS 5-6. On logistic regression analysis, diabetes, HbA1c, collagen-induced large-sized aggregates, and prestroke administration of aspirin remained independent predictors of clinical outcomes in atherothrombotic stroke. In cardioembolic and lacunar stroke, no relations with clinical outcomes were found. Conclusions: High plasma level of HbA1c is involved in enhanced platelet aggregability in acute atherothrombotic stroke patients, and prestroke administration of aspirin may be beneficial to clinical outcomes.