血小板减少性紫癜血小板ATP,ADP释放功能探讨

应用生物发光技术检测血小板减少性紫癜（ITP）患者血小板释放功能，利用磷酸醇及丙酮酸激酶（PEP－PK）将血小板ADP转换成ATP。实验表明ITP患者ATP、ADP释放明显减少（P＜0．05）ATP／ADP比值增大。同时使用肾上腺素（Adr）致聚剂促使血小板聚集，观察聚集后ATP、ADP释放功能的变化。结果提示ITP患者ATP、ADP释放功能明显异常。     

射频消融术前、后血小板聚集功能变化的临床观察

目的　观察射频消融术前、后血小板聚集功能的变化。方法　选择 84例室上性心动过速患者 (男 33例、女 5 1例 ,平均年龄40 .3± 13.8岁 ) ,分成肝素组 ( 4 6例 )和非肝素组 ( 38例 )。分别于术前、术后 1天、2天采外周静脉血 ,测量血小板聚集力 ,同时测量纤维蛋白单体复合物含量。结果　术前两组血小板计数、聚集功能无统计学差异 ( P>0 .0 5 ) ;术后两组血小板计数均有降低 ( P<0 .0 5 ) ;而血小板聚集功能肝素组明显降低 ( P<0 .0 1) ,非肝素组却增高 ( P<0 .0 5 )。术前两组纤维蛋白单体复合物无统计学差异( P>0 .0 5 ) ,而术后两组均增高 ( P<0 .0 5 )。结论　射频消融术可使血小板活性增高 ,使血液处于高凝状态 ,但肝素可抑制血小板聚集 ,对防止发生血栓事件是有益的     

老年慢性呼吸衰竭患者血小板活化因子及血小板功能改变

目的 探讨老年慢性呼吸衰竭患者血小板活化因子（ＰＡＦ）及血小板粘附、聚集、释放功能的改变及与老年慢笥肺心病和呼吸衰竭发展的关系。方法 生物定量法观察老年慢性呼吸衰竭组患者（５５例）、老年健康人组（４０组）及非老年健康人组（３５例）血以激活因子（ＰＡＦ）的改变,放免法观察血以膜ＧＭＰ１４０、血小板释放功能、血小板粘附功能（ＰＡＤＴ）和血小板聚集功能（ＰＡｇＴ）的变化。结果 老年慢性呼吸衰竭组ＰＡＦ为     

噻氯匹定对活化的血小板影响及其临床意义

目的:探讨噻氯匹定增强地尔硫草和5—单硝酸异山梨醇酯抗心肌缺血的疗效及其机制.方法:不稳定型心绞痛常规治疗组(CG)及合用噻氯匹定组(TG)各20例,检查其治疗前、后心肌缺血总负荷和缺血性ST段事件次数;血小板的粘附率、聚集率和血小板计数;血小板膜GP Ⅰ b、GP Ⅱ b和GP Ⅲ a.结果:用药4周时,TG中心肌缺血明显改善;血小板的粘附和聚集功能基本恢复正常,GPⅠb相对含量明显降低,血小板计数明显增加,然而后两项指标未恢复正常(P<0.05);尽管CG中心肌缺血亦有一定程度的改善,但对血小板计数、粘附和聚集功能以及CPⅠb无明显的影响.结论:噻氯匹定具有增强抗心肌缺血的作用,抑制血小板的活性是其主要的机制之一.     

OSAHS患者血小板聚集率和纤维蛋白原的测定

目的　探讨阻塞性睡眠呼吸暂停低通气综合征 (OSAHS)患者血小板聚集率和纤维蛋白原的变化和意义。方法　对 30例OSAHS患者和 32例正常对照者用血小板聚集仪测定血小板的最大聚集率 ,并用双缩脲法测定纤维蛋白原。结果　OSAHS患者的血小板聚集率 (ADP0. 5 μmol/L :32 5 4± 2 3 5 9% ;ADP2 0 μmol/L :5 3 89± 2 1. 14 % )明显高于正常对照者 (ADP0 5 μmol/L :2 1. 0 0± 14 . 85 % ;ADP2 .0 μmol/L :4 0 .2 0± 17. 31% ) (P <0 .0 5 )。OSAHS患者的纤维蛋白原 (388± 74mg/dl)与正常对照者 (36 3± 91mg/dl)无明显差异 (P >0 . 0 5 )。结论　OSAHS患者高血小板聚集率是引起心脑血管疾病增多的重要内在机制之一。     

2型糖尿病血小板活化物质表达与脑梗死的关系

目的　探讨 2型糖尿病患者血小板活化物质表达与脑梗死的关系。　 方法 　采用流式细胞仪对 76例 2型糖尿病和 3 2例糖耐量减退患者测定血小板活化、血小板与白细胞粘附的表达。　 结果　无论 2型糖尿病组还是糖耐量减退组发生急性脑梗死患者血小板活化、血小板与白细胞粘附水平高于腔隙性脑梗死患者 (P <0 0 5 ) ,后者又高于未发生脑梗死患者 (P <0 0 5 ) ;2组中发生急性脑梗死和腔隙性脑梗死患者血小板活化、血小板与白细胞粘附水平与对照组比较差异有显著性 (P <0 0 5 )。　 结论 　 2型糖尿病和糖耐量减退患者测定血小板活化、血小板与白细胞粘附表达对缺血性脑卒中的早期诊断和病情监测有一定的临床价值     

赖氨匹林与阿斯匹林抗血小板聚集疗效的比较

目的 比较赖氨匹林与阿斯匹林对血小板聚集率和粘附率的影响。方法采用随机单盲法,赖氨匹林组30例.服用赖氨匹林200mg qd×14d;阿斯匹林组30例,服用肠溶阿斯匹林100mg qd×14d,治疗前后测定血小板聚集率和粘附率。结果两组服药后血小板聚集率和粘附率均明显下降(P<0.01)。结论赖氨匹林能够确切降低血小板聚集率和粘附率,疗效与阿斯匹林相似,副作用小。     

抗CD59对眼镜蛇毒因子介导的男性冠心病及健康成年人血小板的影响

目的 :研究补体激活对男性冠心病 (CHD)及健康成年人血小板的作用及抗CD5 9对该作用的影响。方法 :应用眼镜蛇毒因子 (CVF)活化血小板 ,通过测定男性CHD及健康成年人血小板的聚集及释放曲线 ,观察抗CD5 9应用前后CVF对血小板变形、聚集及释放功能的影响。结果 :CVF能诱导男性CHD及健康成年人血小板显著、持久的变形和释放 ,但不能诱导血小板聚集。当CVF浓度在 12 .5～ 5 0 .0g/L范围内 ,各组血小板的最大变形幅度与CVF浓度的对数呈线形相关 ,回归方程于CHD组 (36例 )为Y =2 8.717lgX - 19.798(r =0 .95 6 ,P<0 .0 1) ;健康成年人组为Y =2 6 .0 88lgX - 15 .5 81(r =0 .970 ,P <0 .0 1)。抗CD5 9能增强CVF诱导的血小板的最大变形幅度 ,并与剂量相关 ,其血小板最大变形幅度CHD组及健康成年人组分别为空白对照时的 1.39和1.36倍 (P <0 .0 1)。同时抗CD5 9也促进补体诱导的血小板ATP分泌增多。但两组间血小板对CVF及抗CD5 9的反应差异无统计学意义。结论 :活化的补体能诱导男性CHD及健康成年人血小板发生变形、释放 ,但不诱导血小板的聚集 ,且抗CD5 9能增强补体诱导的血小板功能改变     

无症状性脑梗死患者血小板参数及功能的变化

目的 观察无症状性脑梗死(SCI)患者血小板参数及功能的变化.方法 SCI和正常对照组各47例,用全自动血细胞分析仪检测血小板计数(PLT)、平均血小板体积(MPV)、血小板分布宽度(PDW)、大血小板比率(P-LCR)的变化;用不同诱导剂测定血小板最大聚集率;血浆血栓烷B2(TXB2)和(6-keto-PGF1α)的水平用ELISA法测定.结果 SCI患者的MPV、PDW、P-LCR均高于正常对照组,且差异显著(P＜0.001);两组PLT差异无显著性(P＞0.05);SCI患者血小板最大聚集率均显著高于正常对照组(P＜0.001);SCI组TXB2水平显著高于正常对照组(P＜0.001),而6-keto-PGF1α水平则显著低于正常对照组(P＜0.001).结论 血小板参数的改变及血小板功能亢进是SCI发生的危险因素,血小板参数及功能的测定,对于预防SCI发展为有郑状性脑梗死具有重要的参考价值.     

阿司匹林抑制老年冠心病患者血小板聚集的疗效观察

目的:观察阿司匹林治疗老年冠心病患者24周对血小板聚集功能的影响。方法:选择临床需要服用阿司匹林抗血小板治疗,且ADP诱导的血小板聚集率增高的老年冠心病患者122例,给予阿司匹林100mg口服24周。用药前及用药6、12、24周后分别测定血小板聚集率。结果:服用阿司匹林后,患者的血小板聚集率显著降低,6、12、24周测定血小板聚集率与基线比较均差异有统计学意义(均P<0.01),血小板聚集抑制率分别为-(21.13±21.66)%,-(29.25±21.67)%,-(22.87±21.92)%。12周的血小板聚集率较6周进一步下降,但24周较12周则明显升高,两个差值均差异有统计学意义(均P<0.05)。结论:阿司匹林可明显降低患者的血小板聚集功能,但抗血小板聚集作用在24周后较12周有明显下降。     

Correlation between Serum IgG, Platelet Membrane IgG, and Platelet Function in Hypergammaglobulinaemic States

S ummary . Platelet membrane IgG levels were measured by the complement lysis inhibition test, and were correlated with serum IgG levels in 29 patients with elevated immunoglobulins due to multiple myeloma, benign monoclonal gammopathy, systemic lupus erythematosis, rheumatoid arthritis, benign hypergammaglobulinaemic purpura and systemic infection. Platelet membrane IgG was increased in proportion to the elevation of serum IgG with a highly significant correlation coefficient (0.5615, P ≤0.01), irrespective of the underlying disease state. Further washing of the platelets did not significantly alter the amount of membrane bound IgG. Qualitative platelet defects were present in nine of the 10 myeloma patients in whom platelet aggregation, platelet factor 3 availability, platelet adhesion to glass beads and bleeding times were studied. The most severe abnormalities occurred in those patients having the highest levels of platelet membrane IgG. Platelet function was normal despite markedly elevated platelet bound IgG in one patient with benign hypergammaglobulinaemic purpura. These findings indicate that elevation of serum IgG must be excluded before inferring the presence of platelet autoantibodies in patients with elevated platelet bound IgG. They also support the concept that the qualitative platelet abnormalities seen in multiple myeloma result from platelet coating by abnormal immunoglobulins or are secondary to myeloma effect on bone marrow.     

A Comparison of Platelet Size, Platelet Count, and Platelet 35S Incorporation as Assays for Thrombopoietin

SUMMARY. Average platelet size, platelet count, and ³⁵S-incorporation into platelets were compared as methods for the measurement of thrombopoietin-stimulated thrombopoiesis. In mice injected with rabbit anti-mouse platelet serum (RAMPS) average platelet size was shown to be increased as mice were recovering from thrombocytopenia. Also, ³⁵S-measurements on platelets of these mice showed significant increases in cpm/average platelet 2–4 days after RAMPS treatment. Significant increases in ³⁵S-incorporation into the total circulating mass of platelets were found on days 3–4. In normal mice or mice in rebound-thrombocytosis injected with thrombopoietin, platelet size remained unchanged, whereas the platelet count and ³⁵S-incorporation into platelets were shown to be significantly increased. Moreover, a dose-response experiment in mice pretreated with RAMPS showed a slight increase in platelet count as the dose of TSF was increased, but platelet sizes were unaltered. The %³⁵S-incorporation into platelets showed a significant linear dose-response, i.e. as the dose of thrombopoietin was increased, an increase in %³⁵S-incorporation into platelets was observed. These data indicated that of the three indirect measurements of thrombopoietin, the %³⁵S-incorporation into mouse platelets was the most sensitive, followed by platelet counting; the least sensitive measurement of thrombopoiesis was change in platelet size.     

Platelet reactivity, fibrinogen and smoking

40 young healthy male volunteers (20 habitual smokers and 20 non-smokers) were investigated with respect to platelet reactivity, plasma fibrinogen and coagulation factor VIII. Smokers had significantly lower systolic blood pressures and higher venous platelet counts. The results for ADP-induced platelet aggregation, plasma concentrations for the 2 alpha-granule proteins, beta-thromboglobulin and platelet factor 4, did not differ between the 2 study groups involved; nor was there any difference between serum thromboxane B2 formation or plasma factor VIII:C activity. However, as compared to non-smokers, plasma fibrinogen levels were significantly higher among the smokers.     

Effects of 3-Azidothymidine on Platelet Counts, Indium-111-Labelled Platelet Kinetics, and Antiplatelet Antibodies

Treatment of the acquired immunodeficiency syndrome with 3-azidothymidine (zidovudine; AZT) can induce severe neutropenia and anemia, while platelet counts increase. In order to understand the mechanism by which this favorable effect on platelets is induced, we prospectively studied platelet kinetics and platelet serology in 8 hemophiliacs receiving the drug. All patients underwent a second investigation after 3 months of treatment. Four patients were thrombocytopenic before treatment. Platelet counts increased significantly already after 1 week of treatment (p = 0.03), when only 3 patients remained thrombocytopenic. In these latter patients a further increase of platelet counts was noticed during the following 3 months. Platelet life-span was shortened in all patients at the initial investigation and a significant prolongation was measurable at the second evaluation (p = 0.015). Platelet-associated immunoglobulin G was increased in 3 patients at the first investigation and in 4 patients at the follow-up. Platelet-associated complement (PAC3d) was elevated in all subjects at the first determination. It decreased in 6, but increased in 2 patients thereafter; thus these changes did not become significant (p = 0.078). Immunofluorescence studies revealed antiplatelet antibodies in 7 patients' sera before treatment, and in 5 sera during drug therapy. At both investigations, the antibodies bound to the platelet glycoprotein IIIa as was demonstrated by immunoprecipitation of radiolabeled platelet proteins. We conclude, that AZT treatment improves platelet counts in HIV-infected hemophiliacs primarily by a prolongation of platelet survival without having a significant influence on antiplatelet antibody binding.     

β-Thromboglobulin, Platelet Production Time and Platelet Function in Vascular Disease

Plasma beta-thromboglobulin (beta TG) levels were measured in 103 healthy controls and 112 patients suffering from either peripheral vascular disease (PVD), or cerebrovascular disease (CVD) or deep vein thrombosis (DVT). Plasma beta TG was significantly elevated in 46 PVD patients and 24 recent DVT patients compared to controls, but did not differ significantly in 18 chronic DVT and 24 old CVD patients. In addition, heparin neutralizing activity (HNA) and platelet aggregation induced by adenosine diphosphate, 1-epinephrine and thrombin were compared in 33 out of the 46 PVD patients to 33 controls. The mean HNA was significantly shorter in the PVD patients than in controls. The rate and extent of platelet aggregation were increased in PVD patients compared to controls, but the difference was not statistically significant. Platelet production time (PPT) was measured in 20 controls, 35 PVD patients, nine chronic DVT and 12 chronic CVD patients; significantly shorter PPT was only observed in 14 patients with advanced PVD compared to controls, suggesting increased platelet consumption in these patients. All four assays (plasma beta TG, HNA, platelet aggregation and PPT) were performed in 25 patients; no correlation between the four tests was found in these patients suggesting that the tests were measuring various aspects of platelet function. These results suggest that in vivo platelet consumption as well as platelet aggregation and 'release reaction' are presumably enhanced in PVD and recent DVT patients and that plasma beta TG and PPT assays may be better and more specific indicators of in vivo platelet activation than in vitro platelet aggregation test.     

New Platelet Antigen, Siba, Involved in Platelet Transfusion Refractoriness in a Japanese Man

Siba, a new platelet-specific alloantigen involved in a case of platelet transfusion refractoriness is reported. The IgG platelet alloantibody was detected in a multiply transfused patient of Japanese extraction (Sib), by the presence of HLA antibodies. After transfusion of HLA-compatible platelets, the patient suffered from refractoriness. Adsorption studies with pooled lymphocytes showed that the serum contained anti-platelet activity. Family studies indicate that Siba is inherited as an autosomal codominant trait and separate from HLA and Baka. As of this report, segregation from Zw(PlA) and Yuk (Pen) antigen systems have not yet been determined. The gene frequency of Siba in the Japanese population is estimated to be 0.136.