原发性高血压与血管内皮细胞功能障碍

在原发性高血压发病机制中,血管内皮细胞功能障碍起着重要作用,两者互为因果,本文综述了原发性高血压中内皮细胞的损伤机制、检测与治疗机制。     

通心络胶囊对血管内皮损伤的保护作用

血管内皮细胞单层衬于血管的腔面,易受心血管疾病因素作用和损伤刺激,导致内皮细胞功能障碍、紊乱及损伤。这种损伤既是动脉粥样硬化发生的始动环节,也是多种心血管疾病发生和恶化的基础。通心络胶囊由人参、水蛭、     

高尿酸血症与血管内皮细胞功能障碍的研究进展

高尿酸血症,作为一种代谢性疾病,其与高血压、心血管疾病、慢性肾脏病以及代谢综合征之间关系密切。目前的研究发现高尿酸血症带来的氧化应激损伤、炎症细胞和因子的激活、肾素-血管紧张素-醛固酮系统激活、一氧化氮合成减少等病理机制可能参与了血管内皮细胞功能障碍。而且这些机制并不是独立作用,其间还存在着相互影响,相互促进。因此对于高尿酸血症机制的研究,将加深人们对高尿酸血症的认识,以实现早期干预,这对改善血管内皮细胞功能,降低相关疾病的发病率,改善预后具有重要的临床意义。     

血管内皮功能障碍与冠状动脉疾病的关系及防治进展

血管内皮作为循环血液与血管平滑肌之间的中介组织，不仅仅是一层半透性屏障，而且还具有多种重要的生理功能，内皮细胞分泌多种血管活性物质，对维持血管壁张力、血液的流动、管壁的炎症修复和血管的增生具有重要的作用，是功能活跃的代谢组织。内皮细胞损伤会引起内皮功能障碍，与高血压、动脉粥样硬化、心力衰竭等心血管疾病的发生、发展有密切关系。本文就血管内皮功能、血管内皮细胞功能障碍与冠状动脉（冠脉）疾病的关系以及内皮功能保护措施做一综述。     

内皮微颗粒是评估高血压血管内皮细胞损伤的新指标

血管内皮细胞功能障碍是高血压血管损伤的临床重要标志之一.因此,检测血管内皮细胞功能对于高血压的预防、诊治及预后评估具有重要的临床价值[1].内皮微颗粒(endothelial microparticles,EMP)是细胞激活、损伤或凋亡时从内皮细胞的细胞膜脱落下来并携带来自内皮细胞某些抗原特性的微颗粒,其直径为0.2～...     

活血化瘀类中药对血管内皮细胞作用的研究进展

内皮细胞遍布全身心脏血管内膜,是最大的内分泌器官.内皮细胞功能障碍是多种心血管疾病的发病基础,并与呼吸、生殖、神经内分泌、肿瘤、风湿性疾病等有密切的关系.血瘀证与血管内皮损伤有着密切联系,并利用活血化瘀药可以调节血管内皮细胞的内环境及其分泌功能,从而调节内皮功能.     

钙通道阻滞剂与高血压血管内皮依赖性舒张功能

血管内皮细胞具有重要的生理功能,内皮功能不全与高血压病理生理过程密切相关.维护内皮功能的完整性对于预防心血管疾病事件的发生有重要的作用.由于血管内皮细胞上没有电压依赖性钙通道表达,因而钙通道阻滞剂(CCB)不是通过阻滞内皮细胞电压依赖性钙通道起作用.CCB可能通过对抗氧自由基和超氧阴离子对内皮的损伤,增加内皮细胞释放内皮源性舒张因子(EDRF),改善血管内皮依赖性舒张功能.研究表明:CCB对保护和改善内皮功能、改善心血管疾病预后方面有重要的作用.     

血管内皮细胞功能紊乱与血管老化

血管老化指血管结构和功能的退行性改变,引起动脉硬化,导致循环障碍,是冠心病、心绞痛、心肌梗死、高血压等心血管疾病的病理基础.血管老化的研究目前主要集中在血管内皮细胞以及活性物质改变.本文综述了血管内皮功能障碍以及与动脉粥样硬化等内容.     

黄芪甲苷在心血管疾病中的作用

黄芪甲苷具有广泛的药理作用,其中包括抗糖尿病、抗高血压、抗炎症以及保护心肌抗心力衰竭作用。目前研究表明黄芪甲苷可减少心肌细胞损伤和阻止内皮细胞功能障碍。黄芪甲苷对能量代谢综合征发病机制有不同的药理作用。黄芪甲苷有望成为一种新药用于治疗心血管疾病。     

胰岛素抵抗与内皮细胞病变的联系

血管内皮细胞具有调节血管紧张度、血管通透性及促进血管发生的作用。因此,内皮细胞功能障碍被认为是糖尿病所引起的慢性血管并发症发病的关键因素。但内皮细胞功能障碍也可受胰岛素抵抗的各种表现所影响,如:高血压、血脂紊乱和高糖血症等。因此,内皮细胞功能障碍可能与胰岛素抵抗综合征(IRS)有密切关系,甚至有可能是IRS发生的前兆症状。本文将对关于内皮细胞功能障碍是否是胰岛素抵抗和IRS发病的一个核心机制的假说进行回顾和讨论。一、内皮细胞的功能内皮细胞作为血液与细胞间质之间的“门户”发挥重要的调节作用。内皮细胞还可以维持…     

The clinical significance of endothelial dysfunction

PURPOSE OF REVIEW: Endothelial dysfunction is thought to play a pivotal role in the development, progression, and clinical complications of atherosclerosis. Several recent studies have addressed the clinical implications of endothelial dysfunction for cardiovascular events, atherosclerosis, restenosis, and heart failure. Novel findings with respect to endothelial progenitor cells and their alteration by cardiovascular risk factors are characterized and potential therapeutic interventions to improve endothelial and endothelial progenitor cell function are discussed. RECENT FINDINGS: Over the past 5 years evidence has accumulated from clinical studies for a close association of the degree of endothelial dysfunction and clinical cardiovascular events in patients with cardiovascular risk factors, coronary disease, acute coronary syndrome, or heart failure. Understanding of the mechanisms leading to endothelial dysfunction has improved, including the notion that dysfunctional endothelial nitric oxide synthase, in part due to deficiency of the endothelial nitric oxide synthase cofactor tetrahydrobiopterin, likely plays an important role. Major progress has been made in understanding the role of endothelial progenitor cells, which likely contribute to both ischemia-induced neovascularization and endothelial regeneration after injury. Endothelial progenitor cell function is altered in patients with cardiovascular risk factors. SUMMARY: Recent research on endothelial and endothelial progenitor cell dysfunction supports their clinical significance and has led to important insights in the pathophysiology of cardiovascular disease and at the same time provides an important opportunity to develop novel therapeutic approaches. Endothelial function represents a valuable surrogate endpoint to assess the impact of therapeutic interventions.     

Circulating endothelial and progenitor cells:Evidence from acute and long-term exercise effects

Circulating bone-marrow-derived cells,named endothelial progenitor cells(EPCs),are capable of maintaining,generating,and replacing terminally differentiated cells within their own specific tissue as a consequence of physiological cell turnover or tissue damage due to injury.Endothelium maintenance and restoration of normal endothelial cell function is guaranteed by a complex physiological procedure in which EPCs play a significant role.Decreased number of peripheral blood EPCs has been associated with endothelial dysfunction and high cardiovascular risk.In this review,we initially report current knowledge with regard to the role of EPCs in healthy subjects and the clinical value of EPCs in different disease populations such as arterial hypertension,obstructive sleep-apnea syndrome,obesity,diabetes mellitus,peripheral arterial disease,coronary artery disease,pulmonary hypertension,and heart failure.Recent studies have introduced the novel concept that physical activity,either performed as a single exercise session or performed as part of an exercise training program,results in a significant increase of circulating EPCs.In the second part of this review we provide preliminary evidence from recent studies investigating the effects of acute and long-term exercise in healthy subjects and athletes as well as in disease populations.     

Homocysteine, a risk factor for cardiovascular disease

Fasting hyperhomocysteinemia is an independent risk factor for coronary artery disease, stroke, peripheral vascular atherosclerosis, and for arterial and venous thromboembolism. The risk for cardiovascular disease with homocysteine is similar to conventional risk factors. The interaction of hyperhomocysteinemia with hypertension and smoking is strong and the combined effect is more than multiplicative. The combined effect of homocysteine and cholesterol is additive. Homocysteine produces atherosclerosis, thromboembolism, and vascular endothelial cell injury. Vascular dysfunction produced by homocysteine may be due to endothelial cell damage. Homocysteinemia-induced atherosclerosis is probably due to various factors including endothelial cell injury, inability to sustain S-nitroso-homocysteine formation because of imbalance between production of nitric oxide by dysfunctional endothelium and homocysteine, smooth muscle cell proliferation, and thromboembolism. There is strong evidence that endothelial cell injury is associated with oxidative stress produced by homocysteine. Hyperhomocysteinemia is associated with numerous conditions, including coronary disease, stroke, peripheral vascular disease (carotid artery and cerebrovascular atherosclerosis), venous thrombosis, renal disease, diabetes mellitus, and organ transplant. Folic acid, vitamin B₁₂ and B₆ have been shown to be beneficial in reducing plasma homocysteine levels. Folic acid is specifically very effective, safe and inexpensive.     

Asymmetric dimethylarginine as a marker of metabolic dysfunction and cardiovascular disease

Substantial effort has been devoted to the prevention of cardiovascular diseases through modifiable lifestyle factors, but more innovation is needed to better understand mediators of disease progression and to ultimately improve risk prediction. Markers of endothelial dysfunction and oxidative stress may contribute to the underlying processes of atherosclerosis and premature coronary heart disease. Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, has emerged as a potential novel marker of cardiovascular disease. Accumulation of ADMA leads to endothelial dysfunction and initiates and promotes processes involved with atherogenesis. Plasma ADMA levels have been associated with coronary heart disease, diabetes, hypertension, stroke, and peripheral arterial disease. ADMA may be an important link between endothelial dysfunction and cardiovascular disease risk and progression. This review discusses the current literature on ADMA as a novel marker of metabolic dysfunction and cardiovascular disease.     

Circulating endothelial cells in cardiovascular disease

Quantification of circulating endothelial cells (CECs) in peripheral blood is developing as a novel and reproducible method of assessing endothelial damage/dysfunction. The CECs are thought to be mature cells that have detached from the intimal monolayer in response to endothelial injury and are a different cell population to endothelial progenitor cells (EPCs). The EPCs are nonleukocytes derived from the bone marrow that are believed to have proliferative potential and may be important in vascular regeneration. Currently accepted methods of CEC quantification include the use of immunomagnetic bead separation (with cell counting under fluorescence microscopy) and flow cytometry. Several recent studies have shown increased numbers of CECs in cardiovascular disease and its risk factors, such as unstable angina, acute myocardial infarction, stroke, diabetes mellitus, and critical limb ischemia, but no change in stable intermittent claudication, essential hypertension, or atrial fibrillation. Furthermore, CEC quantification at 48 h after acute myocardial infarction has been shown to be an accurate predictor of major adverse coronary events and death at both 1 month and 1 year. This article presents an overview of the pathophysiology of CECs in the setting of cardiovascular disease and a brief comparison with EPCs.     

Circulating endothelial cells in cardiovascular disease.

Quantification of circulating endothelial cells (CECs) in peripheral blood is developing as a novel and reproducible method of assessing endothelial damage/dysfunction. The CECs are thought to be mature cells that have detached from the intimal monolayer in response to endothelial injury and are a different cell population to endothelial progenitor cells (EPCs). The EPCs are nonleukocytes derived from the bone marrow that are believed to have proliferative potential and may be important in vascular regeneration. Currently accepted methods of CEC quantification include the use of immunomagnetic bead separation (with cell counting under fluorescence microscopy) and flow cytometry. Several recent studies have shown increased numbers of CECs in cardiovascular disease and its risk factors, such as unstable angina, acute myocardial infarction, stroke, diabetes mellitus, and critical limb ischemia, but no change in stable intermittent claudication, essential hypertension, or atrial fibrillation. Furthermore, CEC quantification at 48 h after acute myocardial infarction has been shown to be an accurate predictor of major adverse coronary events and death at both 1 month and 1 year. This article presents an overview of the pathophysiology of CECs in the setting of cardiovascular disease and a brief comparison with EPCs.     

Clinical implications of endothelial dysfunction

Endothelial dysfunction is increasingly recognized as an early event in the pathogenesis of cardiovascular disease. This observation is consistent with the growing appreciation of the role of endothelium in maintaining cardiovascular health. Endothelial dysfunction and coronary artery disease are both linked to hypertension, hypercholesterolemia, diabetes mellitus, and cigarette smoking. Modification of these conditions improves both endothelial function and coronary artery disease outcomes. Dietary and lifestyle modifications and antioxidant vitamin supplementation have a beneficial effect on endothelial function, as do angiotensin-converting enzyme inhibitors and lipid-lowering agents. Future studies will determine whether interventions that specifically target endothelial dysfunction can reduce rates of clinical disease.     

Circulating Endothelial Cells and Endothelial Progenitor Cells in Obstructive Sleep Apnea

Increased circulating endothelial cells (CECs) have been observed in patients with vascular injury associated with acute myocardial infarction, pulmonary hypertension, and congestive heart failure. Decreased circulating endothelial progenitor cells (EPCs) have been observed in patients with risk factors for cardiovascular disease. Obstructive sleep apnea (OSA) is associated with increased risk of cardiovascular disease and endothelial dysfunction. Subjects were recruited from patients referred for overnight polysomnograms; 17 subjects had OSA and 10 control subjects did not have OSA. All subjects lacked vascular disease and risk factors for vascular disease. Peripheral blood was obtained from fasting subjects in the morning, following sleep studies. CECs and EPCs were quantified using magnetic bead separation with UV epifluorescence microscopy and flow cytometry immunophenotyping, respectively. Cell counts and demographic variables were compared using unpaired t tests. Regression analysis was performed comparing cell counts with the apnea-hypopnea index (AHI) and nadir SaO(2). Subjects with OSA and controls did not differ significantly in terms of age and body mass index. Subjects with OSA had higher AHI, lower nadir SaO(2), and greater sleepiness (Epworth Sleepiness Scale scores). There were no significant differences in CEC (7.0+/-1.5 vs. 4.9+/-0.9, p>0.05) or EPC (1077+/-318 vs. 853+/-176, p>0.05) between controls and OSA cases, respectively. In this small study, we found no differences in CECs or circulating EPCs between patients with OSA and controls. OSA may not be associated with these markers of vascular endothelial cell injury in patients with no concomitant vascular disease.     

Endothelial dysfunction: its role in hypertensive coronary disease

PURPOSE OF REVIEW: Coronary artery disease is the major cause of death worldwide. Hypertension is a major risk factor for developing coronary disease. It is now recognized that endothelial dysfunction is an early marker of coronary artery disease before structural changes to the vessel wall are apparent on angiography or intravascular ultrasound and that it has a prognostic value in predicting cardiovascular events in hypertensive patients. This review addresses recent developments in hypertension-induced endothelial dysfunction. RECENT FINDINGS: Hyperaldosteronism causes endothelial dysfunction independent of high blood pressure. Exaggerated exercise blood pressure response has been related to endothelial dysfunction. Cyclosporin-A-induced endothelial dysfunction is related to reduced cholesterol content in caveolae. Chronic kidney disease induces changes in caveoli-1 and thus contributes to the reduced nitric oxide bioavailability, and causes oxidative stress independent of the high blood pressure. Asymmetric dimethylarginine plays a role in endothelial dysfunction in hypertensive patients independent of insulin resistance. 20-Hydroxyeicosatetraenoic acid is an independent predictor of hypertension in postmenopausal women. Endothelial dysfunction precedes and predicts the development of hypertension in postmenopausal women. Oral treatment with L-arginine improves endothelial dysfunction in hypertensives and lowers the blood pressure. SUMMARY: The pathophysiology of endothelial dysfunction in hypertension is multifactorial. Recent findings have contributed to our understanding of mechanisms of endothelial dysfunction and support a role for early intervention to prevent irreversible vascular and organ damage.     

Erectile dysfunction: a disease marker for cardiovascular disease

Previous studies have shown an increased incidence of erectile dysfunction (ED) among patients diagnosed with cardiovascular disease (CVD). Both conditions, which may be a consequence of underlying endothelial dysfunction, share many risk factors such as hypertension, dyslipidemia, diabetes, depression, obesity, and cigarette smoking. Because vascular disturbance of the penile endothelium leads to ED, the possibility arises that ED may be an early indicator for systemic endothelial dysfunction and subsequent CVD. Recognizing ED as a disease marker for CVD may help to identify individuals at risk for having a premature cardiovascular event.