急性缺血性脑卒中患者白细胞对血小板聚集的影响及一氧化氮释放

目的探讨缺血性脑卒中患者白细胞与血小板的相互作用及其在中风发病过程中的作用机制和临床意义.方法分别测定40例急性缺血性中风患者富血小板血浆(PRP)加患者白细胞前后和加正常人白细胞前后的血小板聚集率和一氧化氮(NO)含量,同时作白细胞、血小板计数.结果患者白细胞、血小板数和健康对照组无显著差异.加白细胞前,患者血小板最大聚集率和NO含量明显高于对照组(71.63±14.82)%对(63.23±14.30)%(t=2.491,P＜0.05)和(0.386±0.026)μmo1/L对(0.292±0.020)μmo1/L(t=17,407,P＜0.001),加患者白细胞后,血小板最大聚集率为(51.71±15.02)%,明显抑制(t=5.971,P＜0.001),NO浓度为(0.496±0.072)μmol/L,明显升高(t=9.091,P＜0.001),且血小板聚集抑制和NO升高呈负相关.加正常白细胞后的血小板聚集率和NO浓度分别为(67.39±16.62)%和(0.391±0.028)μmol/L,均无明显变化(t=1.205,P＞0.05和t=0.826,P＞0.05).结论缺血性脑卒中患者白细胞激活后通过释放NO对血小板聚集起抑制作用,并和梗死大小、病情轻重及预后有一定关系.     

小剂量阿司匹林对缺血性脑血管病患者血小板聚集功能的影响

目的 :观察小剂量阿司匹林 (ASA)对ICVD患者血小板聚集功能的影响。方法 :用花生四烯酸 (AA ,5 0 0 μmol·L-1)、二磷酸腺苷 (ADP ,5 μmol·L-1)、肾上腺素 (EPN ,5 μmol·L-1)和胶原 (COL ,2 μg·mL-1)做诱导剂检测ICVD患者服用不同剂量ASA组 ( 2 5、5 0和10 0mg·d-1)的血小板聚集率。结果 :各ASA组对AA、COL诱导聚集的变异系数较大。对AA诱导聚集无显著抑制者的比例分别为2 5mg·d-1组 44 4%、5 0mg·d-1组 2 9 6%、10 0mg·d-1组 2 9% ,其中 5 0mg·d-1组中合并糖尿病的例数较显著抑制者中多。结论 :ICVD患者中小剂量ASA作用个体差异较大 ,部分与自身危险因素有关。提示临床中ASA的效果需要实验室检测并应个体化     

双重抗血小板治疗对急性脑梗死患者血小板-白细胞聚集体的影响

<正> 血小板活化是脑梗死(CI)发生、发展的中心环节之一,而血小板与白细胞黏附形成血小板-白细胞聚集体(PLA)是血小板活化的敏感指标。该研究对采用抗血小板药物治疗前后急性CI患者的PLA情况进行了检测。 1 对象和方法 1.1 观察对象:收集作者医院2008-11-01—2009-10-31住院的急性CI患者98例。人选标准:(1)符合全国第四届脑血管病学术会议修订的诊断标准;(2)发病72 h以内;(3)出现颈内动脉供血区局灶神经功能缺失的症状和体征;(4)经头颅CT或MRI检查证实;(5)排除房颤、感染性心内     

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。     

阿司匹林对缺血性脑血管病患者抗血小板聚集作用的临床观察

阿司匹林是抗血小板聚集药物，广泛应用在心脑血管疾病的治疗和预防。本研究对日服阿刮匹林75mg的68例缺血性脑血管病（ICVD）患者通过测定其血小板聚集率观察阿司匹林的抗血小板聚集作用。     

缺血性脑血管病常用药物对血小板聚集功能的影响

应用比浊法测定了川芎嗪，刺五加，维脑路通，潘生丁，阿斯匹林对２０例脑梗塞病人和１２例健康人的血小板聚集功能的影响。结果显示：不论是正常人还是脑硬塞病人，这些药物在体外都能抑制血小板聚集。其中川芎嗪对血小板聚集抑制作用最强，维脑路通作用最弱。     

急性缺血性脑血管病血小板与白细胞计数相关性研究

本文对１３６例脑梗塞患者血小板和白细胞计数的变化进行了相关分析。结果发现急性期血小板计数显著降低（Ｐ＜０．００１），白细胞计数显著升高（Ｐ＜０．００１），两者呈负相关（Ｐ＜０．０１）。提示脑梗塞急性期测定血小板及白细胞计数对帮助了群脑梗塞患者的病情及预后，可作为监测病情的一项辅助指标。     

活化血小板参与缺血性脑卒中炎症反应机制初探

目的 通过细胞共培养模型初步探讨活化血小板参与缺血性脑卒中炎症反应的机制.方法 分离健康人血小板,以0.8μmol/L二磷酸腺苷(ADP)作用20 min激活.同时设静息血小板做为对照,应用血细胞分析仪检测血小板平均内含物(MAC)浓度;将静息血小板和活化血小板分别与人脐静脉内皮细胞株共培养12 h,同时设ADP对照组(只加入等量ADP,无血小板)和空白对照组,采用RT-PCR法检测人脐静脉内皮细胞炎性细胞因子白介素-1β(IL-1β)、白介素.6(IL-6)、白介素-8(IL-8)、单核细胞趋化蛋白-1(MCP-1)的mRNA表达情况.结果与静息血小板组[(266.80±22.14)g/L]比较,ADP诱导激活的活化血小板MPC值[(231.90±14.63)g/L]减低,差异有统计学意义(P<0.05);RT-PCR检测结果显示活化血小板可以诱导共培养的人脐静脉内皮细胞表达IL-1β、IL-6、IL-8、MCP-1 mRNA,而静息血小板组、ADP对照组和空白对照组均无上述细胞因子的表达.结论 体外活化的血小板能够启动血小板一内皮细胞反应,诱导其表达炎症细胞因子,是缺血性脑卒中炎症反应发生的可能机制之一.     

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.     

Clopidogrel High-on-Treatment Platelet Reactivity in Acute Ischemic Stroke Patients

Background

During the first days following an acute ischemic stroke, a consistently good antiplatelet effect of clopidogrel is important due to the increased risk of recurrent ischemia. However, the platelet inhibitory effectiveness of clopidogrel is variable for multifactorial reasons. We investigated the prevalence and risk factors for clopidogrel high-on-treatment platelet reactivity (clopidogrel-HTPR) in acute ischemic stroke patients.

Methods

Using multiple-electrode impedance aggregometry (MEA), the antiplatelet effectiveness of clopidogrel in patients with acute ischemic stroke was prospectively evaluated. Measurements were performed 48 h after therapy was either initiated or continued after hospital admission. Clopidogrel-HTPR was defined as ADP-induced values > 47 U.

Results

A total of 159 patients (71.8 ± 9.8 years, 69 female) were enrolled and 44% (n = 70) patients were clopidogrel-HTPR. 35 of the clopidogrel-HTPR were retested within one week and 57.1% (n = 20) showed a good clopidogrel response during subsequent testing. We identified diabetes mellitus (36.3% vs. 54.4%, p-value = 0.003) and higher HbA1c values (6.3% vs. 6.8%, p = 0.007) as risk factors for clopidogrel-HTPR. Multivariate regression analysis revealed that diabetes mellitus more than doubled the risk of clopidogrel-HTPR (OR 2.41; 95%-CI 1.19-4.88; p = 0.015).

Conclusions

Clopidogrel-HTPR was found in 44% of the patients with acute ischemic stroke. Besides time-dependency of the clopidogrel effect, major risk factors for clopidogrel-HTPR were diabetes mellitus and higher HbA1c values. Further investigations are required to analyse if a function test guided strategy has the potential to optimize the antiplatelet therapy of acute stroke patients.     

The Effects of COVID-19 on Patients with Acute Ischemic and Hemorrhagic Stroke

ObjectiveThe objective of this study was to evaluate how COVID-19 affects patients with acute ischemic or hemorrhagic stroke outcome.Materials and methodsThis retrospective study was performed on adult patients (> 18 years old) with stroke (ischemic or hemorrhagic) who were admitted to hospital with or without COVID-19. The primary outcome was stroke-related disability, which was measured by mRS at baseline and discharge. Hospital duration, intensive care unit (ICU) admission, and mortality were considered the secondary outcomes.ResultsFrom February 2019 until August 2020, we recruited and analyzed 151 patients, 42 of whom had COVID-19 based on RT-PCR tests or lung CT scan findings. COVID-19 positive patients had higher baseline and final mRS scores than the control group (4.46 ± 0.67 vs 4.79 ± 0.61, P: 0.001, 3.83 ± 1.22 vs 4.46 ± 0.67, P: 0.001). Moreover, stroke patients with COVID-19 experienced a more severe disease and required a higher rate of ICU admission (17 vs 0, P:0.001) and longer hospitalization compared to those without COVID-19 (8.50 ± 7.86 vs 7.5 ± 11.20, P: 0.021). Also, mortality was higher in the COVID-19 group (19 vs 13, P:0.001). There was not any significant differences between the two groups in terms of the involvement of cerebral arteries and type of stroke. Male sex, COVID-19, and ICU admission were the main independent risk factors for death.ConclusionThe results of the study showed stroke patients (ischemic or hemorrhagic) with COVID-19 can have more disabilities and incur more hospital complications and mortality than non-COVID-19 patients.     

依达拉奉治疗急性缺血性卒中的临床观察

目的探讨羟自由基清除剂依达拉奉(必存)治疗急性脑梗死患者的临床疗效.方法将60例急性脑卒中病人随机分为治疗组与对照组各30例,两组均用欣易通治疗,治疗组加用必存,对照组加用胞磷胆碱.两组病人分别在入院时、3周后及3月后进行Bathel指数(BI)总分及日常生活活动能力(ADL)积分的评定并进行比较.结果治疗组在3周时(P<0.05)及3月时(P<0.01)BI总分改善方面均优于对照组,3月时两组的有效率分别为86.67%和76.67%,治疗组更佳(P<0.05),在ADL改善方面,治疗组亦明显优于对照组(P<0.05).结论必存对急性缺血性卒中患者有一定疗效.     

东菱克栓酶治疗急性缺血性卒中疗效评价

目的探讨东菱克栓酶(东菱迪芙)对急性缺血性卒中患者神经功能缺损评分的改善作用以及对纤维蛋白原和血小板的影响.方法将110例急性脑卒中病人随机分为治疗组80例与对照组30例.治疗组采用东菱迪芙治疗,对照组采用血塞通注射液治疗.两组病人分别在入院时、3周后进行神经功能缺损评分及纤维蛋白原、血小板的评定与检测,并在3月后进行神经功能缺损评分的随访,进行比较.结果东菱迪芙组在3周时(P<0.05)及3月时(P<0.01)神经功能缺损评分改善方面均优于对照组,3月时两组的有效率分别为93.75%和76.67%,治疗组更佳(P<0.01),3周时治疗组在降低纤维蛋白原方面优于对照组(P<0.01),对血小板计数无影响(P>0.05).结论东菱迪芙对急性缺血性卒中患者有确切治疗作用.     

急性缺血性脑卒中患者外周血白细胞CD11b、CD18表达变化研究

目的　探讨急性脑卒中患者外周血白细胞黏附分子 CD1 1 b、CD1 8的表达 ,以及其在急性缺血性脑损伤发生、发展中的作用。方法　采用流式细胞术 ,用单克隆抗体标记定量测定 3 2例急性脑卒中患者发作 2 4h内外周血白细胞 CD1 1 b、CD1 8的表达量 ,以平均荧光强度 (MFI)的大小来表示 CD1 1 b、CD1 8的相对含量 ,在发病72 h、7d后再分别测定 1次。以 40例健康者作对照。结果　发病 2 4h内患者组白细胞表面黏附分子 CD1 1 b、CD1 8的表达显著高于对照组 (P <0 .0 1 ) ;在发病 72 h内患者组 CD1 1 b、CD1 8的表达逐渐降低 ,但仍高于对照组 (P<0 .0 5 ) ;发病 7d后 ,其结果与对照组相比差异无显著性 (P >0 .0 5 )。结论　急性脑卒中发病时 ,白细胞被激活 ,黏附分子 CD1 1 b、CD1 8表达上调 ,介导白细胞与内皮细胞黏附增强 ,可能会加重缺血后迟发性神经元死亡的病理生理过程。     

Inhibitory Effects of P2Y12 Receptor Antagonist on PAR1- and PAR4-AP-Induced Platelet Aggregation in Patients with Stroke or TIA

ObjectivesThe inhibitory effects of P2Y12 receptor antagonist on PAR1- and PAR4-activating peptide (AP)-induced platelet aggregation have not been fully elucidated. The present study aimed to investigate the inhibitory effects of P2Y12 receptor antagonist on PAR1- and PAR4-AP-induced platelet aggregation using platelet-rich plasma (PRP) from individuals including patients with stroke or transient ischemic attack (TIA).Materials and MethodsPRP was given to 10 healthy individuals pretreated in vitro with cangrelor, then stimulated with adenosine diphosphate (ADP), PAR4-AP, or PAR1-AP. Moreover, 20 patients were enrolled from 148 consecutive patients with acute ischemic stroke or TIA admitted to our institute between December 2017 and April 2019. PRP obtained from each patient before and >7 days after initiation of clopidogrel was similarly stimulated with these agonists. Platelet aggregation was measured using an automatic coagulation analyzer in all participants.ResultsIn healthy individuals, ADP- and PAR4-AP-induced platelet aggregations were significantly inhibited depending on the cangrelor concentration in vitro, while PAR1-AP-induced platelet aggregation was slightly inhibited. In patients with stroke or TIA, clopidogrel inhibited ADP-induced platelet aggregation at all concentrations, and significantly inhibited PAR4-AP-induced platelet aggregation at 50 µmol/L of PAR4-AP (p<0.05), especially in 5 patients who showed high reactivity to PAR4-AP. PAR1-AP-induced platelet aggregation was also slightly inhibited.ConclusionsWe showed significant inhibitory effects on PAR4-AP-induced platelet aggregation by clopidogrel in patients with stroke or TIA who had high reactivity to PAR4-AP.     

尤瑞克林治疗高龄急性脑梗死患者疗效观察

【摘要】 目的 观察尤瑞克林治疗高龄急性脑梗死患者（年龄≥75岁）的临床疗效。 方法 收集年龄≥75岁的急性脑梗死患者201例,按随机数字表法分为尤瑞克林组（100例）和对照组（101例）。两组患者根据病情,给予相同的基础治疗,尤瑞克林组在此基础上给予每天0.15 PNA U尤瑞克林（100 ml生理盐水稀释,静脉滴注,qd,共14 d）,对照组给予空白生理盐水100 ml静脉滴注,qd,共14 d。在治疗前及治疗后第14 d,比较两组患者美国国立卫生院卒中量表（National Institute of Health stroke scale,NIHSS）评分和临床总有效率。 结果 与治疗前相比,两组治疗后NIHSS评分均下降（尤瑞克林组：4.55±2.89 vs 2.54±1.96,t=7.261,P=0.002;对照组：4.11±2.56 vs 3.49±2.55,t=7.439,P=0.013）,治疗后尤瑞克林组患者NIHSS评分低于对照组（t=2.093,P=0.023）,临床总有效率高于对照组（84% vs 55%,U=2896,P=0.001）。 结论 尤瑞克林能促进高龄急性脑梗死患者的神经功能恢复,提高疗效,值得临床推广使用。