纤维蛋白原浓度对机采血小板聚集功能的影响

目的：探讨不同血浆纤维蛋白源（FIB）浓度对机采血小板聚集功能（PAGT）的影响。方法：收集80份机采血小板样品,分别在采集后4h和24h检测PAGT和FIB含量,根据FIB浓度（1.5～2.4g/L、2.5～3.4g/L、3.5～4.4g/L、4.5～5.4g/L）将PAGT测定结果分为4组进行比较分析。结果：血小板最大聚集率在4h时FIB浓度为4.5～5.4g/L组明显高于FIB浓度为1.5～2.4g/L和2.5～3.4g/L组;24h时FIB浓度为4.5～5.4g/L组明显低于FIB浓度为1.5～2.4g/L和2.5～3.4g/L组;各组24h均明显低于4h,差异有统计学意义（P〈0.05或P〈0.01）。结论：FIB浓度越高对机采血小板保存期内PAGT影响越大。     

糖尿病患者血小板的粘附与聚集

糖尿病患者血小板的粘附性增加,对各种能引起血小板聚集的因子的敏感性也增高.作者的研究发现,糖尿病患者血清中与因子Ⅷ密切关连的 vonWillebrand 因子(简称 V-W 因子)和因子Ⅷ抗原的浓度显著增高,而因子Ⅷ促凝血活力的浓度无改变。(若以 O 代表凝血活力,A 代表抗原性,则正常因子Ⅷ的 O/A=1,若<1常说明有凝血发生.——译者注)糖尿病患者的 V-W 因子及 A 增多而 O 减少,说明有血管内凝血,或这些因子的生成或破坏不平衡.在血小板聚集问题上,作者从血浆因素及血小板因素     

硝酸酯类药物的抗血小板聚集和粘附作用

硝酸酯类药作为NO供体,通过胞内cGMP水平提高、Ca2+浓度下降来抑制血小板的聚集.这种作用受血管组织、降钙素基因相关肽(CGRP)、前列环素(PGI2)的影响,而与血流动力学耐受无关.阐明此类药物的抗血小板作用机理及其在抗心绞痛效应中所处的地位具有重要意义.     

硝酸酯类药物的抗血小板聚集和粘附作用

硝酸酯类药作为NO供体，通过胞内cGMP水平提高、Ca^2 浓度下降来抑制血小板的聚集，这种作用受血管组织，降钙素基因相关肽（CGRP）、前列环素（PGI2）的影响，而与血流动力学耐受无关。阐明此类药物的抗血小板作用机理及其在抗心绞痛效应中所处的地位具有重要意义。     

NIDDM病人血小板聚集、第Ⅷ因子相关抗原的临床研究

本文对23例初发Ⅱ型糖尿病(NIDDM)病人进行口服降糖药吡磺环已脲(glipizide)治疗前后的血小板聚集、第Ⅷ因子相关抗原(ⅧR:Ag)和纤维蛋白原进行动态研究。结果表明:NIDDM病人在临床未发现微血管病变时已有血小板聚集率升高,血小板聚集率与空腹血糖、糖化血红蛋白A_1(GHbA_1)无关,与ⅧR:Ag呈明显正相关。glipizide治疗后血小板聚集率明显下降,提示血小板功能异常可能参与NIDDM微血管病变的发生;内皮损害会加剧血小板聚集功能,glipizide对抑制血小板聚集功能有一定作用。     

短暂性脑缺血发作患者血小板聚集功能改变的初步观察

观察短暂性脑缺血发作 (ＴＩＡ)患者发作期和缓解期血小板聚集功能的变化 ,为抗血小板药治疗ＴＩＡ提供客观依据。1　资料和方法ＴＩＡ组 2 0例 ,其中男 15例 ,女 5例 ,年龄 43～ 82岁 ,平均6 3岁。诊断依据符合 1995年全国第四次脑血管病学术会议修订的诊断标准。正常对照组 2 0名 ,男 13名 ,女 7名 ,年龄42～ 74岁 ,平均 6 1岁。检测前 2周内未使用过抗血小板药物。分别在发作期和缓解期测定血小板最大聚集率 (ＭＡＲ)。以二磷酸腺苷 (ＡＤＰ ,5 μｍｏｌ/Ｌ)、肾上腺素 (ＥＰＩ ,5 μｍｏｌ/Ｌ)、胶原 (ＣＯＬ ,2ｍｇ/Ｌ)和花生四烯酸 (…     

冠心病患者血小板聚集功能与炎症因子关系的研究

目的:探讨冠心病患者血小板聚集功能与炎症因子的关系.方法:按照标准入选150例住院治疗的冠心病患者及53例查体健康人(正常对照组).冠心病患者在基础治疗相同的情况下按美国心脏病学会/美国心脏病协会(ACC/AHA)治疗指南分为稳定性心绞痛(SAP)组47例(阿司匹林100 mg/d),不稳定性心绞痛(UAP)组50例(阿司匹林100 mg/d+达肝素5000U Q12h皮下注射),急性心肌梗死(AMI)组53例(阿司匹林100 mg/d+氯吡格雷75 mg/d+达肝素5000U Q12h皮下注射).正常对照组和所有患者入院即刻肘静脉取血,测定空腹血糖、血脂全项、血常规、血小板最大聚集率、尿11-脱氢-血栓素B_2含量、血浆高敏C反应蛋白(hsCRP).结果:AMI组血浆hsCRP水平高于UAP组[(15.46±8.22)mg/L,(7.61±6.11)mg/L P<0.01)]、UAP组高于SAP组[(7.61±6.11)mg/L,(4.25±2.95)mg/L P<0.01]、SAP组高于正常对照组[(4.25±2.95)mg/L,(2.07±1.28)mg/L P<0.05],差异均有统计学意义.二磷酸腺苷诱导的血小板最大聚集率在UAP组、AMI组显著高于正常对照组及SAP组(P<0.05),UAP组与AMI组间、SAP组与正常对照组间血小板最大聚集率无显著差异(P>0.05).花生四烯酸诱导的血小板最大聚集率和尿11-脱氢-血栓素B_2含量在各组间均有显著差异(P<0.05).血浆hsCRP水平与二磷酸腺苷诱导血小板最大聚集率呈显著的正相关(r=0.473,P=0.000);与花生四烯酸诱导血小板最大聚集率呈显著的正相关(r=0.434,P=0.000);与尿11-脱氢-血栓素B_2的含量呈显著的正相关(r=0.554,P=0.000).结论:冠心病患者体内炎症反应与血小板活化状态存在紧密关联,两者共同影响着冠心病的严重程度和稳定状态,是评价冠心病临床状态的检测指标,早期有效抗血小板治疗和减轻炎症反应会有效控制急性冠脉综合征的发生发展.     

血液透析对尿毒症患者血小板粘附聚集功能及膜糖蛋白Ib的作用

尿毒症患者的出血倾向主要与血小板功能的障碍有关。血液透析能否改善患者的血小板功能尚有不同观点。本研究通过对尿毒症患者血液透析前后的血小板粘附率（ＡｄｈＲ）,血小板最大聚集（ＭＡ）功能以及膜糖蛋白Ｉｂ（ＧＰＩｂ）的观察来了解血液透析对尿毒症患者血小板功能的影响。１　对象和方法１．１　对象　维持性血透患者３０例。男１６例,女１４例,平均３４９岁。每周透析１０～１２ｈ,采用碳酸氢盐透析液、血仿膜中空纤维透析器。均为原发性肾小球疾病所致尿毒症。对照组为３０例健康献血员。男１３例,女１７例,平均年龄３９…     

Cryopreservation of platelets isolated with the IBM 2997 blood cell separator: a rapid and simplified approach

The equivalent of 5-7 units of platelets, isolated from a single donor with the IBM Blood Cell Processor 2997 using a dual stage separation chamber, was frozen with the cryoprotectant dimethylsulfoxide (DMSO). The DMSO-saline solution was added directly to the platelets, and the platelets were frozen in a polyvinyl chloride plastic bag by storage in a -80 degrees C mechanical freezer. Washing the thawed platelets with a phosphate-buffered sodium chloride-dextrose solution, pH of 5.0, removed about 95% of the DMSO. In vitro freeze-thaw-wash recovery was 80%, and in vivo 51Cr platelet recovery was 31%. Platelet dense body granules were well maintained after freezing, thawing, and washing. This is a safe and effective method of platelet cryopreservation which can be performed in less time than other currently used methods.     

The use of RA 233 in the preparation of platelets,with the blood cell separator

Summary The intravenous administration of the inhibitor of platelet adhesiveness RA 233 to blood donors before and during cell separation did not increase the yield of platelets in the final concentrate.

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Zusammenfassung Die intravenöse Gabe des Inhibitors der Thrombozytenadhäsivität RA 233 vor und während der Zellseparation erbrachte keine Steigerung der Thrombozytenausbeute im Konzentrat.

     

Red blood cells mediate spontaneous aggregation of platelets in whole blood

The influence of red blood cells on spontaneous platelet aggregation (SPA) has been studied ex vivo. Platelet aggregation was quantified by measuring the fall in single platelet count using a new whole blood platelet counter. When aliquots of whole blood and autologous platelet rich plasma (PRP) were roller-mixed at 37 degrees C, a marked fall in platelet count occurred in whole blood due to SPA but platelet count remained almost unchanged in PRP. When blood from healthy young controls, aged 20-35 years, was compared with healthy old controls, aged 48-80 years, and patients with thrombotic complications, the extent of SPA was in the order: thrombotic patients greater than old controls greater than young controls. Prostacyclin and the new stable prostacyclin analogue Iloprost, at 8 nM effectively inhibited SPA. 2-Chloroadenosine (10 microM) which is an inhibitor of ADP-induced platelet aggregation was also an effective inhibitor of SPA. Acetylsalicylic acid (56 microM) and the thromboxane A2 receptor blocker BM13.177 (0.5 microM) only partially inhibited SPA. ADP from red blood cells is suspected to mediate red cell-induced SPA. However, the possibility that the red cells have an important physical role in SPA cannot be ruled out.     

Immunologic aggregation of human blood platelets and its inhibition in vitro

Unwashed human thrombocytes are best suitable for the immunological activation in PBS-glucose solution. The immunological aggregability of the blood platelets increases in this solution up to more than 1 hour. Rabbit-anti-human-Ig-L-chain (chi) or -anti-human-C1q serum aggregate once washed thrombocytes. The combined application of both antisera has a potencive effect. Soluble human-IgG-rabbit-anti-human-IgG-antibody-F(ab')2-complexes produce a strong thrombocyte aggregation in an intermediate human IgG excess. 4 minutes past heating of human IgG at 63 degrees C a mixture of IgG aggregates (AHGG) arises which activates blood platelets maximally. The AHGG can be stored at -20 degrees C up to at least 4 weeks. Therapeutical aspirin concentrations inhibit the AHGG induced thrombocyte aggregation. Plasma from patients with idiopathic thrombocytopenia inhibits the AHGG mediated platelet aggregation less than plasma from healthy persons.