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1.
目的 观察NO对血管紧张素Ⅱ介导的入球动脉收缩功能的影响,探讨其机制.方法 使用分离的微灌注的入球动脉行等张收缩试验,给予L-NAME及血管紧张素Ⅱ等血管活性物质,观察入球动脉内径的变化.利用NO荧光探针DAF-FM观测入球动脉内皮NO释放情况.结果 L-NAME (10-4mol/L) 时间依赖性的引起入球动脉的收缩,作用60 min后动脉内径减少了35.2 %.在灌注状态下,内皮NO荧光强度持续增加,60 min后达70 %;L-NAME明显抑制内皮NO的释放速率(从29 %降到5.7 %).血管紧张素Ⅱ(10-14 ~ 10-6 mol/L)浓度依赖性的引起入球动脉收缩,最大收缩强度达41 %;L-NAME预处理能够增强入球动脉对于Ang Ⅱ的收缩反应,10-10mol/L Ang Ⅱ收缩动脉直径达46 %(没有L-NAME时为8.5 %),10-8 mol/L时为66 %(没有L-NAME时为41%).结论 灌注产生的血管剪切力是刺激NO释放的重要因素,内皮功能的完整性及NO在调控Ang Ⅱ介导的入球动脉收缩方面发挥重要的作用,NO生物利用度下降可能是肾脏疾病时入球动脉阻力增高的重要机制.  相似文献   

2.
临床与基础医学证据表明,流体剪切力与粥样硬化等动脉病理改变密切相关。在大动脉弯曲或分叉处的血流扰动,可对内皮细胞产生较低且不规则的剪切力,诱导内皮功能障碍和损伤,促进动脉粥样硬化的发生。而在大动脉长、直段的层流所产生的高且规则的剪切力,则保护血管内皮且抑制动脉粥样硬化发生。本文重点关注在动脉粥样硬化的发生发展中,受到剪切力调控并且对疾病引发有关键作用的转录因子或辅助因子,并概述以其为靶点的动脉粥样硬化相关血管病变的防治策略研究。  相似文献   

3.
临床与基础医学证据表明,流体剪切力与粥样硬化等动脉病理改变密切相关。在大动脉弯曲或分叉处的血流扰动,可对内皮细胞产生较低且不规则的剪切力,诱导内皮功能障碍和损伤,促进动脉粥样硬化的发生。而在大动脉长、直段的层流所产生的高且规则的剪切力,则保护血管内皮且抑制动脉粥样硬化发生。本文重点关注在动脉粥样硬化的发生发展中,受到剪切力调控并且对疾病引发有关键作用的转录因子或辅助因子,并概述以其为靶点的动脉粥样硬化相关血管病变的防治策略研究。  相似文献   

4.
<正>施加于内皮细胞的血流剪切力可调控血管平滑肌细胞的表型,对血管稳态维持和动脉粥样硬化发生有重要影响。但这一力学信号由内皮细胞向平滑肌细胞的传递机制待阐明。前期工作中我们发现microRNA可作为信号分子介导内皮细胞与平滑肌细胞的交互作用。我们推测:作用于内皮细胞的流体剪切力通过诱导流场特异性的microRNA分泌,调控平滑肌基因表达和表型转换以及血管功能。利用体外流体剪应力加载模型、共培养合并流体加载模型、小鼠血流扰流模型等研究系统,  相似文献   

5.
血管内皮细胞通透性的变化与人类的许多疾病有关,如动脉粥样硬化、高血压、中风、炎症反应、肿瘤、糖尿病引起的视网膜病变和黄斑水肿等.剪切力是作用于血管内皮细胞的主要力学因素并对血管内皮细胞通透性起重要作用.Rho GTP酶家族是细胞信号转导通路中的一类重要蛋白,参与血管内皮细胞通透性的调控.研究表明,Rho GTP酶在介导剪切力引起血管内皮细胞通透性变化的过程中起重要的信号传导作用.就剪切力对血管内皮细胞通透性的影响以及Rho GTP酶在其分子机制上的作用进行综述.  相似文献   

6.
血管内皮细胞通透性的变化与人类的许多疾病有关,如动脉粥样硬化、高血压、中风、炎症反应、肿瘤、糖尿病引起的视网膜病变和黄斑水肿等.剪切力是作用于血管内皮细胞的主要力学因素并对血管内皮细胞通透性起重要作用.Rho GTP酶家族是细胞信号转导通路中的一类重要蛋白,参与血管内皮细胞通透性的调控.研究表明,Rho GTP酶在介导剪切力引起血管内皮细胞通透性变化的过程中起重要的信号传导作用.就剪切力对血管内皮细胞通透性的影响以及Rho GTP酶在其分子机制上的作用进行综述.  相似文献   

7.
血管内皮细胞通透性的变化与人类的许多疾病有关,如动脉粥样硬化、高血压、中风、炎症反应、肿瘤、糖尿病引起的视网膜病变和黄斑水肿等.剪切力是作用于血管内皮细胞的主要力学因素并对血管内皮细胞通透性起重要作用.Rho GTP酶家族是细胞信号转导通路中的一类重要蛋白,参与血管内皮细胞通透性的调控.研究表明,Rho GTP酶在介导剪切力引起血管内皮细胞通透性变化的过程中起重要的信号传导作用.就剪切力对血管内皮细胞通透性的影响以及Rho GTP酶在其分子机制上的作用进行综述.  相似文献   

8.
血管内皮细胞通透性的变化与人类的许多疾病有关,如动脉粥样硬化、高血压、中风、炎症反应、肿瘤、糖尿病引起的视网膜病变和黄斑水肿等.剪切力是作用于血管内皮细胞的主要力学因素并对血管内皮细胞通透性起重要作用.Rho GTP酶家族是细胞信号转导通路中的一类重要蛋白,参与血管内皮细胞通透性的调控.研究表明,Rho GTP酶在介导剪切力引起血管内皮细胞通透性变化的过程中起重要的信号传导作用.就剪切力对血管内皮细胞通透性的影响以及Rho GTP酶在其分子机制上的作用进行综述.  相似文献   

9.
血管内皮细胞通透性的变化与人类的许多疾病有关,如动脉粥样硬化、高血压、中风、炎症反应、肿瘤、糖尿病引起的视网膜病变和黄斑水肿等.剪切力是作用于血管内皮细胞的主要力学因素并对血管内皮细胞通透性起重要作用.Rho GTP酶家族是细胞信号转导通路中的一类重要蛋白,参与血管内皮细胞通透性的调控.研究表明,Rho GTP酶在介导剪切力引起血管内皮细胞通透性变化的过程中起重要的信号传导作用.就剪切力对血管内皮细胞通透性的影响以及Rho GTP酶在其分子机制上的作用进行综述.  相似文献   

10.
血管内皮细胞通透性的变化与人类的许多疾病有关,如动脉粥样硬化、高血压、中风、炎症反应、肿瘤、糖尿病引起的视网膜病变和黄斑水肿等.剪切力是作用于血管内皮细胞的主要力学因素并对血管内皮细胞通透性起重要作用.Rho GTP酶家族是细胞信号转导通路中的一类重要蛋白,参与血管内皮细胞通透性的调控.研究表明,Rho GTP酶在介导剪切力引起血管内皮细胞通透性变化的过程中起重要的信号传导作用.就剪切力对血管内皮细胞通透性的影响以及Rho GTP酶在其分子机制上的作用进行综述.  相似文献   

11.
Molecular mechanisms underlying the activation of eNOS   总被引:1,自引:0,他引:1  
Endothelial cells situated at the interface between blood and the vessel wall play a crucial role in controlling vascular tone and homeostasis, particularly in determining the expression of pro- and anti-atherosclerotic genes. Many of these effects are mediated by changes in the generation and release of the vasodilator nitric oxide (NO) in response to hemodynamic stimuli exerted on the luminal surface of endothelial cells by the streaming blood (shear stress) and the cyclic strain of the vascular wall. The endothelial NO synthase (eNOS) is activated in response to fluid shear stress and numerous agonists via cellular events such as; increased intracellular Ca2+, interaction with substrate and co-factors, as well as adaptor and regulatory proteins, protein phosphorylation, and through shuttling between distinct sub-cellular domains. Dysregulation of these processes leads to attenuated eNOS activity and reduced NO output which is a characteristic feature of numerous patho-physiological disorders such as diabetes and atherosclerosis. This review summarizes some of the recent findings relating to the molecular events regulating eNOS activity.  相似文献   

12.
本文利用边界元方法计算了腹主动脉叉。在动脉粥样硬化前后的血液流场、血管壁切应力等血液流体动力学特性,通过对动脉粥样硬化产生前后,左、右髂总动脉壁切应力的计算结果分析,对粥样斑块病变产生和发展的血液流体动力学原因做出了判断。结果显示:腹主动脉叉几何形状的不对称性导致分叉处血液流速、血管壁切应力分布的不对称,内侧壁切应力大于外侧壁,右髂总动脉内侧壁切应力大于左髂总动脉。动脉粥样硬化处由于血管腔变窄血液流速明显变大、切应力变大,容易使斑块表面撕裂出现组织增生,粥样斑块下游处血流速度、切应力减小,形成血液分离区,使血细胞聚集,造成动脉粥样硬化发展、加剧。  相似文献   

13.
目的研究急性无氧功率自行车运动对不同性别人体颈总动脉弹性模量和局部血液动力学的影响。方法以9名男性和8名女性20~30岁年龄段的健康志愿者作为研究对象,使用无氧功率自行车持续进行4组相同强度的急性运动训练。应用彩色超声多普勒分别检测静息状态及每组运动训练后的颈总动脉管径波形、轴心流速波形,用电子自动血压计同步检测心率和血压大小。运用经典血液动力学理论对检测数据进行分析,计算颈总动脉的弹性模量和局部血液动力学参数,包括压力-应变弹性模量、流量率、周向应变、壁面切应力和振荡剪切指数。结果运动后心率增加;随着运动的积累,颈总动脉弹性模量呈增加趋势;一个心动周期内轴心血流速度和流量率最大值与平均值上升,流速和流量率最小值下降;收缩压和平均压增高,舒张压无明显改变;周向应变无明显改变;切应力最大值有明显增加的趋势,切应力最小值下降趋势明显;振荡剪切指数也有增大的趋势。结论急性无氧功率自行车运动可增加20~30岁年龄段不同性别志愿者的颈总动脉弹性模量,并对颈总动脉局部血液运动学和动力学功能参数产生明显的影响。本文结果将为无氧运动调控脑血管功能提供有用的血液动力学信息。  相似文献   

14.
Exercise and vascular adaptation in asymptomatic humans   总被引:1,自引:0,他引:1  
Beneficial effects of exercise training on the vasculature have been consistently reported in subjects with cardiovascular risk factors or disease, whereas studies in apparently healthy subjects have been less uniform. In this review, we examine evidence pertaining to the impact of exercise training on conduit and resistance vessel function and structure in asymptomatic subjects. Studies of arterial function in vivo have mainly focused on the endothelial nitric oxide dilator system, which has generally been shown to improve following training. Some evidence suggests that the magnitude of benefit depends upon the intensity or volume of training and the relative impact of exercise on upregulation of dilator pathways versus effects of inflammation and/or oxidation. Favourable effects of training on autonomic balance, baroreflex function and brainstem modulation of sympathetic control have been reported, but there is also evidence that basal vasoconstrictor tone increases as a result of training such that improvements in intrinsic vasodilator function and arterial remodelling are counterbalanced at rest. Studies of compliance suggest increases in both the arterial and the venous sides of the circulation, particularly in older subjects. In terms of mechanisms, shear stress appears to be a key signal to improvement in vascular function, whilst increases in pulse pressure and associated haemodynamics during bouts of exercise may transduce vascular adaptation, even in vascular beds which are distant from the active muscle. Different exercise modalities are associated with idiosyncratic patterns of blood flow and shear stress, and this may have some impact on the magnitude of exercise training effects on arterial function and remodelling. Other studies support the theory that that there may be different time course effects of training on specific vasodilator and constrictor pathways. A new era of understanding of the direct impacts of exercise and training on the vasculature is evolving, and future studies will benefit greatly from technological advances which allow direct characterization of arterial function and structure.  相似文献   

15.
Nitric oxide (NO) released by endothelial cells in response to hemodynamic shear stress is a key controller molecule of the vascular functions and antiatherogenic mechanisms. Endothelial dysfunction is associated with increased cardiovascular events. Therefore, several indirect techniques have been employed to evaluate endothelial function or NO bioavailability. However, a growing body of evidences suggests limitations of the indirect methods for evaluation of NO bioavailability. In years, it has been considered that NO is immediately oxidized or inactivated in blood stream. However, recent studies suggest that NO remain active in blood stream, causing remote biological response. Therefore, measuring plasma NO concentration directly in the circulation will contribute to clarify the kinetics and physiological roles of NO and to evaluate endothelial function. In this article, the measurement of plasma NO concentration using a newly developed catheter-type NO sensor will be described.  相似文献   

16.
Many cardiovascular diseases are closely associated with hemodynamic parameters. The main purpose of this study is mimicking a physiological blood flow in stenotic arteries to provide an understanding of hemodynamic parameters. An experimental setup was designed to produce original pulsatile flow and measure pressure pulse waves through a compliant tube. Moreover, a numerical model considering fluid–solid interaction was developed to investigate wall shear stress and circumferential stress waves, based on the results of the experiments. Results described elevated mean pressure by increasing stenosis severity especially at the critical obstacle of 50 %, which the pressure rose significantly and raised up by 10 mm Hg that may cause damage in endothelial cells. Increasing in stenosis severity led to: more negative wall shear stress and more oscillation of shear stress at the post-stenotic region and also more absolute value of angular phase difference between wall shear stress and circumferential stress waves at the stenotic throat. All of the aforementioned parameters determinant the endothelial cell pathology in predication of potential sites of progression of atherosclerotic plaques. Therefore, results can be applied in study of plaque growth and mechanisms of arterial remodeling in atherosclerosis.  相似文献   

17.
Local hemodynamic environment, including low shear stress and increased tensile stress, determines the localization, growth and progression of coronary atherosclerosis. As atherosclerotic lesions evolve, the diseased coronary arteries undergo local quantitative and qualitative changes in their wall, and progressively become stiff. Arterial stiffening amplifies the atherogenic local hemodynamic environment, initiating a self-perpetuating vicious cycle, which drives the progression of atherosclerosis and the formation of atherosclerotic plaque. In vivo evidence indicates that endothelial dysfunction is associated with arterial stiffness, an association that creates a challenging perspective of utilizing stiffness as an early marker of endothelial dysfunction and future atherosclerosis. Coronary stiffening is also associated with vascular remodeling, which is a major determinant of the natural history of atherosclerotic plaques. Thus, arterial stiffness may constitute a useful marker for the identification of the remodeling pattern, in particular expansive remodeling, which is closely associated with high-risk plaques. The early identification of endothelial dysfunction, or a high-risk plaque may enable the early adoption of preventive measures to improve endothelial function, or justify pre-emptive local interventions in high-risk regions to prevent future acute coronary syndromes. Further experimental and perspective clinical studies are needed for the investigation of these perspectives, whereas the development of new modalities for non-invasive and reliable assessment of coronary stiffness is anticipated to serve these studies.  相似文献   

18.
It is assumed that critical hemodynamic factors play an important role in the onset, localization and degree of post-operative complications, for example, thrombosis and restenosis. Of special interest are sudden expansion flows, which may occur in straight artery segments such as the common carotid after endarterectomy or end-to-end anastomoses. Sudden expansion geometries are possible origins of early post-operative emboli and significant myointimal hyperplasia resulting in early or late complications. Transient laminar axisymmetric and fully three-dimensional blood flows were simulated employing a validated finite volume code in conjunction with a Runge-Kutta particle tracking technique. Disturbed flow indicators, which may predict the onset of thrombosis and/or restenosis, were identified and employed to evaluate 90 degrees -step and smooth expansion geometries.Smooth expansion geometries have weaker disturbed flow features than step expansion geometries. Specifically, the regions near the expansion wall and the reattachment point are susceptible to both atherosclerotic lesion and thrombi formations as indicated by non-uniform hemodynamic indicators such as near-zero wall shear stress and elevated wall shear stress gradients as well as blood particle accumulation and deposition. A new parameter, the wall shear stress angle deviation (WSSAD) has been introduced, which indicates areas of abnormal endothelial cell morphology and particle wall deposition. In turn, regions of low wall shear stress and high wall shear stress gradients are recognized as susceptible sites for arterial diseases. Thus, it is interesting to note that high WSSAD surface areas cover low wall shear stress, high wall shear stress gradient locations as well as high wall particle deposition.A gradual change in step expansion geometry provides better results in terms of WSSAD values and hence potentially reducing atherosclerosis as well as thrombi formation.  相似文献   

19.
不同型式流体切应力对血管内皮细胞生理生化的影响   总被引:1,自引:0,他引:1  
血管内皮细胞经常处于血液流动力的作用下 ,它能感知血流力的变化 ,在调节血管的功能和结构中起着重要作用。血液流动力的变化与某些血管性疾病的发生发展有着密切的关系 ,因此血液流动力对内皮细胞的影响受到广泛关注。本文就流体切应力对内皮细胞生理、生化影响的研究进展作一简要综述。  相似文献   

20.
内皮细胞应力测试装置   总被引:1,自引:0,他引:1  
目的 通过研制“内皮细胞应力测试装置”,为研究血流动力学环境对人工培养的内皮细胞生物学特性的影响提供实验平台。方法 应用流体力学及血流动力学理论与分析方法,制作了“内皮细胞应力测试装置”。结果 本装置可以精确调控正常生理水平和超生理水平下的切应力值、正应力值、以及脉动波幅和脉动频率。结论 本装置能模拟与人体生理状况较一致的血流动力学环境。  相似文献   

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