急性脑卒中患者血小板超微结构的观察

为了探讨急性脑卒中患者血小板超微结构的变化，采用ＤＸＡ４～１０型电子显微镜对５０例急性脑卒中患者血小板中α颗粒数及每平方微米中血小板α颗粒数进行观察。结果：脑卒中组上述指标显著低于对照组（Ｐ＜０．０１）。其中缺血性脑卒中者降低更显著（Ｐ＜０．００１）。梗塞面积大于５ｃｍ的患者α颗粒较小面积损伤者显著减少（Ｐ＜０．０５），而与梗塞部位无关。血液稀释和阿司匹林（ＡＳＡ）治疗后α颗粒数减少显著改善（Ｐ＜０．０５）。另外还发现，血小板α颗粒减少与血钙减少呈正相关（ｒ≥０．３４，Ｐ＜０．０５）。结果提示，血小板超微结构的改变可作为判断脑卒中诊断、治疗及预后的客观指标。     

急性期脑梗塞患者血小板参数的动态变化及临床意义

观察了８６例急性脑梗塞患者血小板参数的动态变化及其临床意义。结果：脑梗塞组急性期平均血小板体积（ＭＰＶ）和血小板体积分布宽度（ＰＤＷ）均明显高于对照组。梗塞面积越大、病情越重者，血小板ＭＰＶ和ＰＤＷ越增高，且ＭＰＶ和ＰＤＷ两参数与血小板计数（ＰＬＴ）均呈显著负相关。提示此项检查可作为临床上估计病情和梗塞面积的一项指标。     

急性脑梗死患者P选择素的周围血流式细胞分析

目的：探讨Ｐ选择素在急性脑梗死中的变化。方法：采用流式细胞术对４３例脑梗死患者发病１～２天及发病后１０～１４天进行Ｐ选择素的研究。结果：（１）急性脑梗死患者发病后１～３天内其血小板表面Ｐ选择素表达量较对照组显著增高（Ｐ〈０．０１）。（２）发病后１０～１４天内的血小板表面Ｐ选择素表达较对照组增高（Ｐ〈０．０１）。（３）发病后１０～１４天的Ｐ选择素表达量较发病后１～３天显著下降（Ｐ〈０．０１）。结论：Ｐ选择素在急性脑梗死的发病过程中具有重要作用。     

脑缺血病人血小板肌球蛋白轻链激酶和Ca^2＋,Mg^2＋—ATP？…

目的 探讨急性缺血性脑血管病血小板球蛋白轻链激酶（ＭＬＣＫ）和Ｃａ＾２＋Ｍｇ＾２＋－ＡＴＰ酶活性的变化及与血小板胞浆游离钙浓度（Ｃａ＾２＋）ｉ浓度,结果 ＴＩＡ组和脑梗死组ＭＬＣＫ活性与对照组相比均有明显增加（Ｐ〈０．０１）,而Ｃａ＾２＋,Ｍｇ＾２＋－ＡＴＰ酶活性均低于对照组（Ｐ〈０．０５,Ｐ〈０．０１）,ＴＩＡ组和脑梗死组血小板静息（Ｃａ＾２＋）ｉ均高于对照组;血小板静息（Ｃａ＾２＋）ｉ与血小板     

急性脑梗塞患者血小板颗粒膜糖蛋白的动态变化

目的 探讨血小板在脑缺血损害中的作用及血小板颗粒膜蛋白（ＧＭＰ－１４０）的临床意义。方法 对２６例急性脑膜塞患者发病后６ｈ内，２４ｈ，第３天，第７天，第１４天血浆内ＧＭＰ－１４０的水平进行了动态测定。结果 发病后２周的血浆ＧＭＰ－１４０水平均高于正常对照组（Ｐ〈０．０５），发病后６小时内即见血浆ＧＭＰ－１４０水平增高，至第３天达最高水平，以后逐渐降低，第３天ＧＭＰ－１４０水平梗塞灶最大直径呈显著正     

精神分裂症患者氯丙嗪治疗前后血小板聚集功能观察

目的 探讨精神分裂症患者血小板聚集功能及氯丙嗪治疗对血小板聚集功能的影响。方法 对３３例首次住院的男性精神分裂症患者氯丙嗪治疗前后进行ＢＰＲＳ评定及肾上腺素致聚下的血小板聚集功能检测，并与５５名正常对照相比较。结果 精神分裂症患者血小板１分钟聚集率（ＰＡＲ１）、５分钟聚集率（ＰＡＲ５）显著高于对照组（Ｐ〈０．０５，Ｐ〈０．０１）；用氯丙嗪治疗１个月后，患者临床症状缓解，ＢＰＲＳ评定分值下降（Ｐ〈０．０１），血小板聚集功能ＰＡＲ１无显著性改变（Ｐ〉０．０５），ＰＡＲ５明显升高（Ｐ〈０．０１）。结论 精神分裂症患者血小板聚集功能增强；氯丙嗪治疗可导致血小板的激活状态。     

脑梗塞患者血小板膜糖蛋白CD41,CD62p,CD63的监测

用流式细胞术，以单克隆抗体为分子探针，测定了不同病程脑梗塞患者周围血中血小板膜糖蛋白（ＧＭＰ）ＣＤ４１、ＣＤ６２Ｐ和ＣＤ６３的阳性表达率，并与健康人作对照。结果显示病人组３种ＧＭＰ的表达率均显著高于对照组（Ｐ＜０．０１～０．００１）；腔隙梗塞与大面积梗塞两亚组之间３种ＧＭＰ表达率无显著差异；脑梗塞亚急性期和恢复期检测者，其血小板活化程度较急性期检测者为低（ＣＤ４１、ＣＤ６２ＰＰ＜０．０５，ＣＤ６３Ｐ＜０．０１），但与对照组比仍然保持在一个相当高的活化水平上（Ｐ＜０．０５～０．０１）。     

全脑缺血大鼠海马及血液血小板激活因子动态变化的研究

目的 研究血小板激活因子（ＰＡＦ）在急性脑缺血过程中的作用。方法 用高效薄支析法对大鼠全脑缺血后再灌注１、３、６、７２小时因液、海马、大脑顶叶皮质的ＰＡＦ进行了观察。结果 再灌小１小时后海马中ＰＡＦ含量较对照组明显升高（Ｐ〈０．０１）,而３小时时则下降地正常水平（Ｐ〉０．０５）。血液中ＰＡＦ的升高出现较晚,再灌注后３小时旱血中ＰＡＦ明显升高,６小时时最明显,７２小时时与对照组比较仍有显著性差异（Ｐ     

缺血性脑血管病纤维蛋白原和血小板状态的观察

目的　探讨血小板和纤维蛋白原（ＦＩＢ）在脑梗死发病中的作用。方法　观察有血栓倾向的疾病、ＴＩＡ、急性脑梗死患者及正常对照组的血小板计数（ＰＬＴ）、血小板平均体积（ＭＰＶ）、血小板聚集率（ＰｔＡｇｔ）和ＦＩＢ浓度。结果　脑梗死急性期的ＰＬＴ 明显低于正常组和其它疾病组,各疾病组的ＭＰＶ 和ＦＩＢ明显高于正常组,ＰｔＡｇｔ各组无明显差异。ＦＩＢ与欧洲卒中评分（ＥＳＳ）成正相关。结论　血小板和ＦＩＢ的变化出现在脑梗死之前,它们促进了血栓的形成,ＦＩＢ的水平可作为评价病情严重程度的指标之一。     

脑梗塞患者血小板活化部位的探讨

采用ＦＣＭ检测脑梗塞患者（１６例腔梗，１８例大面积梗塞）颈内静脉（Ａ）和肘静脉（Ｂ）的血小板ＧＭＰ－１４０，ＧＰ５３和ＧＰⅡｂ／Ⅲａ。结果：脑梗塞组Ａ和Ｂ血中三种ＧＰ阳性表达率均明显高于非脑血管疾病（ＣＶＤ）组和健康组Ｂ血（Ｐ＜０．０１～０．００１）；脑梗塞组Ａ血明显高于同组Ｂ血（Ｐ＜０．０５～０．００５），Ａ／Ｂ比值为１．２４～２．５２，而非ＣＶＤ组Ａ与Ｂ血之间阳性率无显著差异，Ａ／Ｂ比值≤１．０６；大面积梗塞组Ａ血阳性率高于腔梗组Ａ血（Ｐ＜０．０５），但两组Ｂ血无显著差异。提示脑梗塞急性期血小板主要在脑循环中活化，测定Ａ血指标较测定Ｂ血更能敏感地反映脑梗塞时血小板的活化程度和功能状态。     

Vulnerable plaque imaging

The concept of vulnerable plaque is well established with increasing evidence from clinical and basic research. The paradigm has shifted from focusing exclusively on the hemodynamic effects of plaque (ie, resulting lumenal stenosis alone as a predictor of stroke risk) to assessment of the structure and composition of plaque (eg, denuded endothelium with inflammatory elements as a nidus for platelet-fibrin clumping). It is increasingly evident that methods to detect and characterize vulnerable plaque must be developed and optimized. Although MR imaging, CT, and ultrasound provide data regarding single lesions, future investigations relying heavily on nuclear medicine techniques may offer functional assessment of the entire cardiovascular system.     

The unstable plaque

Ischaemic strokes and transient ischaemic attacks are commonly caused by cerebral embolism originating from formation of a platelet-rich thrombus superimposed on an atherosclerotic plaque or by atherothrombotic plaque rupture in a carotid or intracranial artery. Despite advances made through ultrasound imaging in our understanding of atherosclerotic plaque progression and regression, the issue of whether differences in plaque structure alone can distinguish between lesions that become symptomatic and others that remain clinically silent continues to be debated. Recent biochemical and imaging studies have identified characteristics that may reflect a high risk of vulnerability, such as outward, abluminal plaque remodelling, the presence of intra-plaque haemorrhage, inflammation, severe flow disturbances around the encroaching lesion, plaque cap thinning and ulceration, and abnormal plaque motion. Plaque stability may be improved through management of traditional cardiovascular risk factors or with biological or pharmacological agents that target pathways involved in plaque pathophysiology. Unstable plaques place patients at risk of unpredictable ischaemic events and in patients with such lesions, specific preventive treatment beyond long-term antiplatelet therapy can be used to prevent new or recurrent events.     

The symptomatic carotid plaque

BACKGROUND: The natural histories of equally severe symptomatic and asymptomatic carotid stenoses are very different, which suggests dichotomy in plaque behavior. The vascular biology of the symptomatic carotid plaque is presented in this review. SUMMARY OF REVIEW: Histology studies comparing asymptomatic and symptomatic plaques were identified from MEDLINE. Reports in which stenosis severity was not stated or not similar for symptomatic and asymptomatic patients were excluded. In vitro studies and reports from the coronary circulation were reviewed with regard to the vascular biology of the plaque. Histology studies comparing carotid plaques removed from symptomatic and asymptomatic patients reveal characteristic features of unstable plaques: surface ulceration and plaque rupture (48% of symptomatic compared with 31% of asymptomatic, P<0.001), thinning of the fibrous cap, and infiltration of the cap by greater numbers of macrophages and T cells. In vitro studies suggest that macrophages and T cells release cytokines and proteinase, which stimulate breakdown of cap collagen and smooth muscle cell apoptosis and thereby promote plaque rupture. CONCLUSIONS: Infiltration of inflammatory cells to the surface of carotid plaques may be a critical step in promoting plaque rupture and resultant embolization or carotid occlusion. Further understanding of cell recruitment and behavior in carotid atherosclerosis may allow better detection of unstable plaques and therapeutic methods of plaque stabilization.     

Plaque rupture and plaque erosion

There are multiple substrates for coronary thrombosis overlying an atherosclerotic plaque. The most common, plaque rupture, consists of an interruption of a thin fibrous cap overlying a lipid rich core. Plaque rupture is a result of macrophage infiltration and matrix degradation, is often seen in calcified plaques, and is highly associated with hypercholesterolemia. A less common substrate, plaque erosion, is not associated with elevated cholesterol and is the prime cause of coronary thrombosis in premenopausal women. The characteristic histologic features are abundant surface smooth muscle cells and proteoglycans, and a small or absent lipid rich core. The mechanisms of plaque erosion are unclear, and there are no consistent risk factors, although patients are often smokers.     

Transesophageal echocardiography aortic plaque imaging

Despite some limitations, TEE is a sensitive and specific diagnostic technique for the diagnosis and evaluation of aortic plaque. TEE provides a semi-invasive, portable, and widely available means for assessing aortic plaque and associated embolic risk in patients with embolic events, thus guiding rational therapeutic choices. Improvement in tissue characterization and three-dimensional capabilities may further improve the diagnostic accuracy of TEE for aortic plaque detection and evaluation.     

Carotid endarterectomy for asymptomatic plaque

Statistical correlations are linear noninteractive relationships, but the dynamics of causation are nonlinear and involve complex interactions where variables change through their effect on one another and interact with the context of the patient over time. The discovery and interpretation of plaque vulnerable features in the individual patient are not determined for the asymptomatic patient being considered for carotid endarterectomy. New technologies for identification of plaque chemical and morphologic composition are on the horizon and may be applicable to certain patients but change in their usefulness as the plaque and patient change over time.