血小板与动脉粥样硬化

动脉粥样硬化受多种遗传因素和外界因素的影响,其发病机制与血栓形成、脂质浸润及损伤炎症反应等有关。研究证实,血小板参与动脉粥样硬化的形成,但其机制尚未阐明,可能与血小板激活引起炎症反应、血小板释放细胞因子、血小板介导内皮黏附以及相关脂蛋白调节有关。     

单核细胞/血小板复合体与动脉粥样硬化

在动脉粥样硬化中,单核细胞/血小板复合体(MPA)扮演着重要角色,广泛参与内皮损伤、炎性细胞招募、纤维帽形成和破裂等过程。P选择素、血小板糖蛋白Ⅱb/Ⅲa受体、蛋白激酶受体-1、细胞外基质金属蛋白酶诱导因子等促进了单核细胞/血小板复合体的形成,后者则可通过激活经典的炎症性核因子-κB通路,分泌环氧化物酶-2、组织因子、白细胞介素、肿瘤坏死因子-ɑ等影响动脉粥样硬化的发展。     

血小板致动脉粥样硬化斑块形成的相关研究

在动脉粥样硬化斑块形成和血脂紊乱的基础上,常伴随着血小板的异常激活。血小板参与了动脉粥样硬化斑块形成的全部过程,即血小板本身具有致斑块性,血小板参与体内血脂调节、促炎症及致氧化应激作用。该文介绍血小板致动脉粥样硬化斑块形成的机制和相关临床研究。     

血小板与动脉粥样硬化研究的新进展

在高血脂等多种因素作用下,血小板膜结构和功能发生改变,血小板活化,释放多种血管活性物质,促使内皮细胞、血管平滑肌细胞、巨噬细胞等转化成泡沫细胞,导致动脉粥样硬化的产生和发展.     

载脂蛋白E与动脉粥样硬化

载脂蛋白E是血浆脂蛋白的重要组成成份 ,主要介导血浆脂蛋白特别是乳糜微粒和低密度脂蛋白的代谢与清除 ,在脂蛋白代谢中发挥重要作用。转基因小鼠和基因敲除的小鼠证实了载脂蛋白E在动脉粥样硬化发生发展中的作用。载脂蛋白E通过不同机制对动脉粥样硬化起到一定的抑制作用。     

载脂蛋白与动脉粥样硬化

近年来对载脂蛋白(apo)的研究发展较快,已证实apo的变化比高密度脂蛋白(HDL),低密度脂蛋白(LDL)和极低密度脂蛋白的变化更易检出异常情况,(VLDL)是鉴别动脉粥样硬化(AS)中较血脂更重要的指标。一:载脂蛋的分类目前,apo的分类大多是按各类脂蛋白(Lp)中的主要肽类进行的,当不止一种时,则用罗马数字加以区别。 apoA分为AⅠ、AⅡ、AⅢ、AⅣ,A I占HDL的60～70%。经等电聚焦双向电泳发现,AⅠ有六种分子量大致相等,等电离点(IP)各异的异物体(Isomeride)     

载脂蛋白E多态性与血栓形成性动脉粥样硬化

动脉粥样硬化 (AS)在人类的发生相当普遍。但不是所有的 AS都导致同样的后果或者发生在相同的时期。只有那些易于形成血栓的 AS(脑梗死 ,心肌梗死 ,肺梗死 ,外周动脉梗死 )才是真正的隐患 (是否可以提出良性 AS和恶性 AS的概念 )。如果能够从众多的 AS人群中筛选出易于发生血栓形成的潜在受害者 ,并加以具有针对性的预防和治疗 ,对于个体来说 ,则可以减少发病机会而达到延长寿命和提高生活质量的目的 ;而对于群体来说 ,可以避免不必要的大规模用药而减少卫生资源的浪费和药物不良反应。脂质代谢紊乱与 AS及冠心病有着密切联系 ,而载脂…     

血小板-淋巴细胞相互作用与动脉粥样硬化

动脉粥样硬化是一种慢性炎症性疾病,血小板和淋巴细胞参与其发生、发展的整个过程。血小板和淋巴细胞之间通过直接接触和分泌可溶性介质的方式发生相互作用,进而调节彼此功能,并可形成细胞间聚集体,同时血小板还可促进淋巴细胞在损伤血管壁的募集。血小板-淋巴细胞相互作用影响动脉粥样硬化的进展,有可能成为新的治疗靶点。本文主要针对血小板-淋巴细胞的相互作用及其对动脉粥样硬化的影响进行综述。     

老龄ApoE基因敲除小鼠动脉粥样硬化斑块的病理观察

目的：观察西方饮食喂养的老龄（≥48周）ApoE基因敲除小鼠血管动脉粥样硬化斑块的病理组织学状况。方法：选取6周龄雄性纯合子ApoE基因敲除小鼠30只，均予以西方饮食喂养，分别在喂养42周（48周龄）、54周（60周龄）、66周（72周龄）时，随机各取10只，取无名动脉做病理检测。酶法检测血脂情况，冰冻切片光镜下观察无名动脉粥样硬化斑块病理情况，图像分析管腔及斑块面积，免疫组化染色观察斑块中骨桥蛋白、α肌动蛋白的表达。von Kossa染色观察斑块钙化情况。结果：西方饮食喂养48周龄后，ApoE基因敲除小鼠主动脉弓内形成广泛而且典型的动脉粥样硬化成熟斑块，60周龄时，无名动脉内斑块面积、其与血管面积比率和自发破裂率最高，不稳定斑块比例最大（P〈0．05～〈0．01）。结论：长期西方饮食喂养ApoE基因敲除小鼠，是研究动脉粥样硬化成熟斑块很好的动物模型。     

载脂蛋白与动脉粥样硬化的关系

动脉粥样硬化与脂质(尤其是载脂蛋白)代谢异常有关。目前已知载脂蛋白(Apo)有8种,本文拟浅述ApoA、ApoB与动脉粥样硬化的关系。一、ApoA 已有研究表明,血浆ApoA-Ⅰ含量与动脉粥样硬化呈负相关。ApoA-Ⅰ是体内抗动脉粥样硬化的因素之一,其和高密度脂蛋白(HDL)可将周围组织细胞的游离胆固醇酯化,并转运到肝脏进一步代谢,以防外周组织的脂质沉积和粥样硬化。ApoA-Ⅰ和磷脂结合可加强上述作用,有助于细胞内胆固醇     

Platelet function defects

Summary. Inherited defects of platelet function are a heterogeneous group of disorders that can result in bleeding symptoms ranging from mild bruising to severe mucocutaneous haemorrhage. These defects may be classified according to their effect on the various steps of platelet microthrombi formation including initiation, extension and cohesion, or based on their particular structural or functional deficiency. Platelet membrane receptor deficiencies result in the rare, but well‐characterized syndromes of defective clot initiation, such as Bernard–Soulier Syndrome. Platelet storage pool defects are the most common disorders affecting the extension phase of clot formation. Glanzmann thrombasthenia, with absent or dysfunctional αIIbβ3 receptor is the prototypical defect of the cohesion/aggregation phase of microthrombi formation. Many of these disorders share common treatments although some therapies will have greater efficacy for one patient than another and should be individualized so as to provide optimal control of symptoms. Currently much effort is being put into methods to more rapidly and accurately diagnose patients with platelet disorders and to initiate appropriate therapy and prevent life threatening bleeding.     

Platelet function analysis

Since the last guidelines for BCSH platelet function testing were written in the late 1980s, many new tests have become available. Previously most platelet function tests were traditionally utilized to aid in the diagnosis and management of patients with platelet and haemostatic disorders. Most traditional tests were also largely restricted to the specialized laboratory or centre. However, nowadays there is also much renewed interest in monitoring the efficacy of anti-platelet therapy and measuring platelet hyper-function. A number of dedicated platelet function instruments have now become available that are much simpler to use and are beginning to be utilized as point of care instruments. These can now provide measurement of platelet function within whole blood without the requirement of sample processing. Some are also beginning to be incorporated into routine clinical use and can be utilized as not only as general screening tests of platelet function but to monitor anti-platelet therapy and to potentially assess both risk of bleeding and/or thrombosis. Modern flow cytometric-based platelet function analysis now also provides a wide variety of specific tests that can assess different aspects of platelet biology that are useful for diagnostic purposes. This review will highlight some of these of new tests/instruments and discuss their potential utility both within the haemostasis laboratory but also as potential point of care instruments.     

Platelet function and lipid-lowering interventions

Platelets play an important role in the process of atherothrombosis, and antiplatelet therapy is of proven efficacy in the prevention of vascular events in high-risk patients. In this review, we briefly consider the studies reporting that circulating atherogenic lipoproteins enhance platelet activity. We also evaluate the evidence showing that lipid-lowering interventions (including the use of statins) are associated with the normalisation of platelet activity. This beneficial effect should enhance the anti-atherogenic and anti-thrombotic potential of lipid-lowering interventions.     

Platelet function and lipid-lowering interventions

Platelets play an important role in the process of atherothrombosis, and antiplatelet therapy is of proven efficacy in the prevention of vascular events in high-risk patients. In this review, we briefly consider the studies reporting that circulating atherogenic lipoproteins enhance platelet activity. We also evaluate the evidence showing that lipid-lowering interventions (including the use of statins) are associated with the normalisation of platelet activity. This beneficial effect should enhance the anti-atherogenic and anti-thrombotic potential of lipid-lowering interventions.     

Platelet function in pre-eclampsia

Pronounced hemostatic changes occur during pregnancy, and the balance shifts markedly in favor of hypercoagulability. Although primarily a result of a marked rise in the levels of several procoagulants and a fall in some natural anticoagulants, platelet activation also contributes to this prothrombotic tendency. Several studies have confirmed the accentuation of platelet activation in pre-eclampsia (P-EC), which remains an important obstetric complication affecting ~2 to 4% of pregnancies. Although there is still a long way to go, significant inroads have been made in the understanding of this enigmatic condition. Whereas the pathogenesis of P-EC is protean and involves a complex interplay of placental and maternal tissues, platelet activation is likely to contribute to several clinical features. Several techniques have been used to assess platelet activation in P-EC. Detection of aberrations of platelet function and activation appear to have predictive value for its diagnosis. The findings also lend support to the use of antiplatelet agents as prophylaxis in those women with a high risk of developing the condition.     

Platelet function in hypertension

Platelets from hypertensive patients show increased sensitivity to agonists and have high intracellular free Ca(2+) concentration. Furthermore, in hypertension, platelets show enhanced endogenous production of reactive oxygen species and a reduced antioxidant status which increases protein tyrosine phosphorylation, enhances Ca(2+) mobilization and attenuates NO bioavailability. The study of the abnormalities in platelet function in hypertensive patients can lead to the development of new pharmacological strategies to prevent and/or palliate hypertension-derived complications associated to platelet hyperactivity.