Platelets and Atherothrombosis: An Essential Role for Inflammation in Vascular Disease — A Review

Atherothrombosis is the common link between clinical manifestations of arterial vascular disease including ischemic stroke and acute coronary syndromes, such as unstable angina and acute myocardial infarction. Our understanding of the common pathologic mechanisms underlying these conditions has significantly increased during the past ten years, yet atherothrombosis as the “root cause” of a large proportion of cardiovascular and cerebrovascular diseases is largely underappreciated. Although the classical risk factors of dyslipidemia, smoking, diabetes, hypertension, obesity, and sedentary lifestyle are widely recognized as being associated with a heightened risk of vascular disease, inflammation of the vascular system during the past decade has become increasingly regarded as the principal underlying mechanism in the development of clinical atherothrombotic disease. In addition, platelet-derived inflammatory mediators play an essential role in the pathogenesis of cardiovascular disease, being involved at all stages of plaque development until their eventual rupture and subsequent formation of a platelet-rich thrombus. Mounting evidence supports the role of both localized and systemic inflammation in these events. Platelets are central to vascular inflammatory processes. Thus, inflammation can stimulate local thrombosis and thrombosis can amplify inflammation. Consequently, antiplatelet therapy for the prevention of serious vascular events may provide a double benefit via an anti-inflammatory action of the antiplatelet agent in modifying plaque formation and stability and antiplatelet activity that inhibits platelet aggregation and thrombus formation from occurring following plaque rupture.     

The Role of Essential Fatty Acids in Alcohol Dependence and Tissue Damage

Evidence for the role of essential fatty acids in alcohol dependence is reviewed. If alcohol-induced tissue damage is associated with impaired fatty acid and phospholipid metabolism, supplements of essential fatty acids might be beneficial in the treatment of alcoholics. The evidence for this effect is examined.     

Silent Cerebrovascular Damage and Its Early Correlates in Essential Hypertensive Patients

This study tested the association between cognitive functions, cerebrovascular damage, and cerebrovascular reactivity in 71 essential young hypertensives (age matched) and 22 normotensives (age matched). They underwent ambulatory blood pressure monitoring, neurocognitive tests, cerebral magnetic resonance, and transcranial Doppler. Twenty-three percent of patients showed more than 10 white matter lesions and 8% showed none. No control subjects showed more than 10 white matter lesions and 90% of normal controls showed no lesions. Patients with more than 10 white matter alterations had longer hypertensive story and showed significant lower nocturnal blood pressure fall. Pulsatility index was correlated with the number of white matter lesions.     

内皮素-1与原发性高血压

原发性高血压时血浆内皮素-1水平升高,可导致外周阻力增加,并且通过激活ETA和ETB受体可加重高血压病心、肾、动脉系统的损害,形成恶性循环。ETA/ETB受体阻滞剂或选择性的ETA受体阻滞剂均能使全身血压下降,保护高血压病的靶器官。     

血管内皮细胞损伤在脓毒症大鼠心肌损伤中的作用

目的 探讨血管内皮细胞损伤与脓毒症心肌损伤之间的关系.方法 将30只大鼠随机分为假手术组、脓毒症组和乌司他丁组,分别用酶联免疫法吸附法检测血浆中血管性血友病因子(vWF)、血栓调节素(TM)浓度,罗氏生化仪检测血浆肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)水平,心导管检测心脏左心室压力(LVP)、左心室压力上升或下降最大速率(+ dp/dtmax或-dp/dtmax)来评价心功能,用免疫印迹法检测心肌脑利钠肽(BNP)水平来评价心肌损伤情况.结果 脓毒症组vWF、TM浓度较假手术组明显增加,同时伴有以CK、CK-MB升高为标志的心肌损伤加重,以及BNP表达增加和LVP、+dp/dtmax、-dp/dtmax的降低为标志的心功能下降,乌司他丁组内皮细胞损伤降低,心肌损伤减轻以及心功能改善.结论 内皮细胞损伤可能是脓毒症引起心肌损伤的重要原因.     

原发性高血压合并2型糖尿病患者肾素前体表达水平及与血管损伤的相关性

目的　探讨原发性高血压合并2型糖尿病患者肾素前体表达水平及与血管损伤的相关性。方法　入选原发性高血压患者78　例，原发性高血压合并2型糖尿病患者41例。采集病史，并进行血压、颈-股动脉脉搏波传导速度的测量及生物化学指标的检查，应用酶联免疫吸附法测定患者血浆肾素前体浓度，应用SPSS　19.0统计软件进行分析，应用t检验比较两组间各指标均数是否具有统计学差异，采用Pearson相关分析肾素前体与颈-股动脉脉搏波传导速度及各指标的相关性，运用多元线性回归分析脉搏波传导速度的独立相关因素。结果　两组间年龄、体质指数、舒张压、脉压、肌酐、总胆固醇、甘油三酯、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇的差异无统计学意义（P>0.05）。原发性高血压合并2型糖尿病组收缩压、空腹血糖、甘油三酯均高于原发性高血压组，差异有统计学意义（P<0.05）。原发性高血压合并2型糖尿病组肾素前体与原发性高血压组相比差异无统计学意义（P>0.05），原发性高血压合并2型糖尿病组颈-股动脉脉搏波传导速度值高于原发性高血压组，差异具有统计学意义（P<0.05）。对颈-股动脉脉搏波传导速度的相关因素进行分析显示，年龄、收缩压、脉压与颈-股动脉脉搏波传导速度相关（P<0.05），多元线性回归分析显示颈-股动脉脉搏波传导速度与年龄、收缩压独立相关（P<0.05）。结论　（1）原发性高血压合并2型糖尿病患者血浆肾素前体水平与原发性高血压患者无差异。（2）原发性高血压合并2型糖尿病时血管损伤加重，但与肾素前体间未见明确相关性。     

血管内皮功能紊乱在高尿酸血症肾损害中的作用

目的探讨血管内皮功能紊乱在高尿酸血症肾损害发病机制中的作用。方法将36只雄性Wister大鼠随机分为对照组、高尿酸血症模型组(模型组)和苯溴马隆治疗组(治疗组),每组12只。应用氧嗪酸钾(尿酸酶抑制剂)联合高酵母饲料建立高尿酸血症肾损害大鼠模型,治疗组在建立高尿酸血症模型基础上加用苯溴马隆(立加利仙)降尿酸治疗,对照组给予普通饲料及等量蒸馏水灌胃,于2、4、6周末自大鼠颈静脉窦取血,检测血尿酸、肌酐水平。6周末处死全部大鼠,取肾组织进行HE、Masson染色,观察肾脏病理改变并测量肾间质纤维化面积,检测肾间质小管内皮型一氧化氮合酶、内皮素1、低氧诱导因子1α表达。结果 2周末,模型组血尿酸水平较对照组及治疗组明显升高;6周末,模型组血肌酐水平较对照组及治疗组明显升高,而后两组之间无明显差异。模型组肾间质纤维化面积较对照组及治疗组均显著增加,模型组大鼠肾组织内皮型一氧化氮合酶表达明显低于对照组及治疗组,而内皮素1及低氧诱导因子1α表达均明显高于对照组及治疗组。结论血尿酸水平升高可减少肾间质小血管内皮型一氧化氮合酶合成并促进内皮素1表达,从而影响肾间质血管内皮功能,通过缺血缺氧机制导致肾间质纤维化。     

Herpesvirus Antibodies and Vascular Complications in Essential Hypertension

ABSTRACT. Antibodies against herpes simplex virus (HSV) and cytomegalovirus (CMV) were examined in sera from 132 patients with essential hypertension and 54 normotensive healthy subjects of the same age and sex. Prevalences of HSV and CMV antibodies (titre ≥4) were equal in patients and controls. A HSV antibody tire ≥4 was found in 39.5% (17/53) of patients with WHO stage III hypertension, in 26.2% (22/85) of patients with stage I–II hypertension, and in only 9.4% (5/54) of normotensive subjects (p<0.0005). The HSV antibodies were mainly of type 1. No association between CMV antibodies and vascular complications could be demonstrated.     

Rapamycin Prolongs Survival and Arrests Pathophysiologic Changes in Murine Systemic Lupus Erythematosus

Objective. To evaluate the effects of oral rapamycin (RAPA), a macrolide immunosuppressant that has been shown to interfere with T cell activation events, on the course of spontaneous disease progression in the MRL/MpJ/lpr/lpr (MRL/I) mouse model of lupus. Methods. RAPA treatment (6, 12, or 25 mg/kg 3 times per week) was evaluated by monitoring survival rates, autoantibody levels, and urinary albumin levels. Additionally, concanavalin A responsiveness, interleukin-2 (IL-2) production, lymphoid organ size, and histopathology were evaluated ex vivo. Results. RAPA prevented the typical rise in anti–double-stranded DNA antibody and urinary albumin levels and prolonged survival. Spleen and lymph node sizes were significantly decreased, inflammatory changes in the lung, liver, kidney, spleen, lymph node, and thymus were significantly reduced, and T cell mitogen–stimulated splenocyte proliferation and IL-2 production were restored. Conclusion. Data from 3 independent experiments demonstrated that RAPA significantly reduced or prevented many pathologic features of lupus normally seen in the MRL/1 mouse, and suggest that RAPA may be useful as a therapeutic agent in SLE in humans.     

系统性红斑狼疮严重血液系统损害的治疗

血液系统损害是系统性红斑狼疮（systemic lupuserythematosus,SLE）最常见的临床表现之一,也是SLE的诊断标准之一。白细胞减少及血小板减少是SLE疾病活动性指数中用来评价疾病活动度的指标。SLE活动性测定中也以红细胞压积、白细胞计数、淋巴细胞计数及血小板计数作为评价疾病活动度的指标。几乎所有患者在病程中均会出现一种或几种血细胞学异常。     

NDM-1 and the Role of Travel in Its Dissemination

Antimicrobial resistance is a growing problem globally. The appearance and spread of bacteria that are resistant to most or all commonly available antibiotics has raised the specter of untreatable bacterial infections. The New Delhi metallo-beta-lactamase-1 (NDM-1) has received wide attention because of the extreme resistance it confers, its presence in many common pathogens, its rapid spread to multiple continents, and local nosocomial spread in some areas. Most early reports of infections were in individuals who had received medical care in the Indian subcontinent. This paper will explore the role of travelers in the movement of pathogens and microbial genetic material associated with resistance, with a special focus on the appearance and dispersal of bacteria carrying this mobile genetic element, bla _NDM-1, and the contributing factors, including growing long-distance travel and expansion of travel across international borders for medical, dental, and surgical care (medical tourism).     

高血压血管重塑及药物干预后的逆向重塑

高血压血管重塑是近几年来随着基础心血管病学研究发展提 出的高血压靶器官损害中的一种新机制,它既是高血压的重要病理变化,又是高血压维持、 恶化的结构基础。随着人们对高血压重塑认识的深入,高血压病的临床治疗目标已从仅限于 控制血压水平,提高到了逆转血管重塑的高度。本文就高血压血管重塑定义、特点、评估方 法以及抗高血压治疗后的逆向重塑作一综述。     

谷氨酸受体在学习、记忆中的作用及其与血管性痴呆的关系

谷氨酸是中枢神经系统内的重要神经递质,通过与其受体作用,调节正常脑内几乎所有的功能,包括学习和记忆。血管性痴呆是脑血管病引起的获得性智能损害综合征,学习和记忆障碍是其主要表现。许多研究表明,各种谷氨酸受体都与学习和记忆关系密切。因此,谷氨酸受体可能从分子水平上参与了血管性痴呆的发病机制。