吸烟对血小板功能的影响与动脉粥样硬化的关系

多数学者认为,吸烟可通过多种因素导致动脉粥样硬化的发生.其中吸烟对血小板功能的影响在动脉粥样硬化的发生中具有重要作用。     

妊高征血管内皮细胞功能紊乱研究进展

妊高征是严重影响母儿健康的妊娠期特有疾病。学者们对妊高征的研究迄今已逾百年 ,但其病因和发病机理仍未彻底阐明。其间提出不少妊高征发病学说 ,但均或多或少存在缺陷 ,尚不能全面透彻地解释妊高征发病机理。由于病因不清 ,对妊高征的防治造成困难。近年来 ,对妊高征的研究取得了很大的进展 ,尽管仍未能解决病因问题 ,但理论得到更新 ,认识更加深入。血管内皮细胞损伤学说的提出是妊高征研究的转折点1　血管内皮细胞功能血管内皮不只是简单的屏障作用 ,更有重要的内分泌功能 ,参与血管损伤的修复 ,维持凝血 /抗凝平衡 ,甚至参与免疫反应…     

吸烟鼠脑血管内皮细胞间粘附分子1的表达在动脉粥样硬化形成中的作用

为观察吸烟对大鼠脑血管内皮细胞超微结构、细胞间粘附分子 1表达的影响 ,建立大鼠吸烟动物模型 ,将 75只大鼠随机分为长期大量组、长期小量组、短期大量组、戒烟组和对照组 ,免疫组织化学和原位杂交结合显微图像分析系统检测大鼠脑血管内皮细胞细胞间粘附分子 1的表达 ;电镜观察内皮细胞超微结构的改变。结果发现 ,吸烟大鼠脑血管内皮细胞细胞间粘附分子 1表达增加 (P <0 .0 5 ) ,与吸烟量和时程存在剂量—效应关系 ;内皮细胞超微结构改变显著。戒烟鼠细胞间粘附分子 1表达下调 (P >0 .0 5 ) ,内皮细胞超微结构病理改变明显恢复。结果提示 ,吸烟致脑血管内皮细胞细胞间粘附分子 1表达上调可能是吸烟导致动脉粥样硬化的分子机制之一。     

动脉粥样硬化与内皮细胞功能障碍

血管内皮是一重要的功能性界面,不仅具有调节血管舒缩的功能,而且还参与了动脉粥样硬化的发生与发展。在多种影响内皮细胞功能的因素中,氧化损伤是导致内皮细胞功能障碍的主要原因。     

内皮细胞功能异常与动脉粥样硬化的研究进展

血管内皮细胞参与构成人体的生理屏障和维持人体内环境稳态,并且为适应内环境的动态变化及满足人体不同组织新陈代谢的需要,不同组织的内皮细胞具有功能差异性和组织特异性.心脏血管内皮细胞参与维持心脏内环境的稳定,当内皮细胞因高脂血症、高血糖、氧化应激、炎症反应及其他代谢因素发生功能障碍,会参与心血管疾病的病理生理过程,例如动脉...     

内皮细胞和神经系统间相互作用与动脉粥样硬化

神经系统对心血管系统的调节作用十分重要。通过神经或神经一体液途径，神经系统可影响或改变血管内皮细胞和平滑肌细胞的功能状态，并率与动脉粥样硬化的病理发生。本文就神经系统血管调节功能的修饰作用进行了综述。     

内皮细胞粘附分子与动脉粥样硬化

内皮细胞是血液单核细胞、淋巴细胞迁移到内皮下层的功能屏障和中介。在过氧化脂质、病毒感染等动脉粥样硬化危险因子作用下,内皮细胞粘附性发生改变,其表面粘附分子呈异常表达,诱导单核细胞粘附并向内皮下层迁移。通过检测内皮细胞的粘附性、抑制粘附分子表达或封闭粘附分子可为动脉粥样硬化的早期诊断与防治提供新的思路。     

内皮细胞凋亡与动脉粥样硬化

内皮细胞凋亡在动脉粥样硬化形成过程中起重要作用。多种影响动脉粥样硬化的因素均影响内皮细胞凋亡。血管内膜损伤使内皮细胞凋亡增加,影响血管调节功能,促进平滑肌细胞增殖、迁移和血液凝固,因此内膜损伤可能启动动脉粥样硬化事件。对内皮细胞凋亡的研究将为揭示动脉粥样硬化的发生机制奠定基础。     

吸烟与血管内皮损伤

越来越多的体内和体外研究表明 ,吸烟会损伤血管内皮 ,发生冠心病的危险性增加。至于香烟引起内皮损伤的具体成分以及机制尚未阐明     

Cigarette smoking and atherosclerosis in autopsied men.

The association of cigarette smoking and atherosclerorosis was investigated in 1320 autopsied men, 25--64 years of age. Aortic and coronary lesions were evaluated visually in coded specimens and objectively by analysis of radiographs. Using schedules that had been tested on pairs of living persons, interviewers obtained estimates of cigarette smoking habits of the deceased men from surviving relatives. Data were analysed for black and white men in the total sample of cases and also in groups according to the presence (selected disease group) or absence (basal group) of diseases thought to be associated with smoking (emphysema, lung cancer, etc.) or with coronary heart disease (myocardial infarction, hypertension, diabetes, stroke, etc.). Atherosclerotic involvement of aorta and coronary arteries was greatest in heavy smokers and least in nonsmokers for both races in the total sample of cases, the basal group and the selected disease group.     

血管内皮功能障碍与动脉粥样硬化

血管内皮不仅是血液与内皮下组织的屏障,还具有内分泌功能.当血管内皮功能障碍时,会引起一系列的病理生理反应,导致动脉粥样硬化.在内皮功能障碍向动脉粥样硬化演变的过程中,血管紧张素Ⅱ和氧化型低密度脂蛋白起重要作用.内皮细胞损伤时,机体自身的修复机制发挥作用,相关药物可改善内皮功能,稳定动脉粥样硬化,改善预后.内皮细胞功能的...     

Primary endothelial dysfunction: atherosclerosis

The endothelium synthesizes and releases several vasodilating factors, including nitric oxide, endothelium-derived hyperpolarizing factor, and prostacyclin. Under certain conditions, it also liberates vasocontracting factors. Thus, the endothelium plays an important role in regulating vascular homeostasis. Several intracellular mechanisms are involved in the synthesis of nitric oxide, including receptor-coupled G proteins, the availability of L-arginine, cofactors for endothelial nitric oxide synthase and the expression of the enzyme. Endothelial dysfunction by aging, menopause and hypercholesterolemia is involved in the development of atherosclerotic vascular lesions, and predisposes the blood vessel to several vascular disorders, such as vasospasm and thrombosis. Multiple mechanisms are apparently involved in the pathogenesis of the endothelial dysfunction in atherosclerosis. The reduced production of nitric oxide by the endothelium is caused by abnormalities in endothelial signal transduction, availability of L-arginine, cofactors for endothelial nitric oxide synthase and expression of the enzyme. Other mechanisms may also be involved in the impaired endothelium-dependent relaxations in atherosclerosis, including increased destruction of nitric oxide by superoxide anion, altered responsiveness of vascular smooth muscle, and concomitant release of vasocontracting factors. In addition to the treatment of the underlying risk factors, several pharmacological agents can improve endothelial dysfunction in atherosclerosis. Thus, the endothelium is a novel therapeutic target for the treatment of atherosclerotic cardiovascular disease.     

Obstructive sleep apnea syndrome, endothelial dysfunction and coronary atherosclerosis

In obstructive sleep apnea syndrome (OSAS), repetitive episodes of apnea cause increased sympathetic nerve activity, increased surges in arterial blood pressure, swings in intrathoracic pressure, oxidative stres, hypoxia and hypercapnia. The association of OSAS with some diseases, having endothelial dysfunction in their physiopathology, such as hypertension, diabetes mellitus, obesity, coronary artery diseases, stroke and heart failure is common. Increased sympathetic nerve activity and also endothelial dysfunction which are the results of hypoxia, have important roles in vascular complications of OSAS. When compared with healthy population, an important endothelial dysfunction in OSAS patients and relationship between OSAS severity and endothelial dysfunction have been shown. In this review, the relationship between OSAS and endothelial dysfunction was overviewed.