微重力对血管内皮细胞生物学特性的影响

微重力状态下,人体将表现出一系列的心血管去适应性反应.由于血管内皮细胞是血管壁最重要的组成部分,因此血管内皮细胞生物学特性的改变将与去适也性反应直接相关.研究微重力状态下血管内皮细胞生物学特性的改变对预防和治疗航天员心血管的去适应性反应尤为重要.     

微重力对血管内皮细胞生物学特性的影响

微重力状态下,人体将表现出一系列的心血管去适应性反应.由于血管内皮细胞是血管壁最重要的组成部分,因此血管内皮细胞生物学特性的改变将与去适也性反应直接相关.研究微重力状态下血管内皮细胞生物学特性的改变对预防和治疗航天员心血管的去适应性反应尤为重要.     

模拟微重力对机体内皮细胞、血小板功能的影响

重力状态的改变将引起机体一系列生理机能的异常,如心血管系统中血液的重新分布、骨骼系统中骨质破坏的增加、造血系统中造血组织的减少等.人类登月计划的顺利实现以及空间站的成功建立,为研究微重力状态下机体生理功能的改变开启了新的篇章.随着模拟微重力仪的研发更是使这一领域出现了飞速的发展,但关于微重力状态下机体凝血功能的改变还有...     

微重力影响造血干/祖细胞生物学特性及其机制研究进展

造血干/祖细胞具有自我更新、增殖及多向分化的功能,从而使机体维持正常的造血.机体在微重力环境下会出现外周血细胞数量和功能的改变,其中有多方面的原因,而在微重力环境下造血干/祖细胞生物学特性的改变是这一改变的主要因素.对微重力如何影响造血干/祖细胞的迁移、增殖及分化等生物学特性进行了综合评述.     

内皮祖细胞的动员、归巢和分化

内皮祖细胞是内皮细胞的前体细胞 ,在某些生理、病理状态下可随血流至相应组织 ,分化为内皮细胞 ,并进一步形成血管。内皮祖细胞不仅参与胚胎发育的血管发生 ,而且在成人机体的血管新生中起重要的作用。研究内皮祖细胞的生物学特性、动员、归巢及分化机制将为临床治疗缺血性疾病、创伤修复及抑制肿瘤生长提供理论依据。     

尾部悬吊大鼠胸主动脉、肺动脉超微结构变化的动态观察

目的 观察模拟微重力时大小循环动脉血管超微结构重塑随时间变化的差异,为微重力后立位耐力降低的机制研究积累资料.方法 用透射电镜观察-30°尾部悬吊7 d(TS7组)、14 d(TS14组)及对照组大鼠胸主动脉、肺动脉壁超微结构的变化.结果 TS7组胸主动脉内皮细胞表面出现绒毛状突起,部分线粒体空泡变性,内皮下基膜有分层,内弹力板较厚,且厚度不均匀,内弹力板下出现大量的胶原纤维;TS14组胸主动脉内皮细胞变性较明显,部分内皮细胞基质致密化,基膜复层化,内弹力板有破碎,弹力纤维增多.TS7组肺动脉部分内皮细胞突起,细胞内出现脂滴,内皮细胞基膜出现分层状改变,弹力板变薄、断裂,其下方可见收缩型平滑肌及合成型平滑肌细胞;TS14组肺动脉内皮细胞空泡变性较明显,内弹力板未见明显改变,弹力板内外均可见较多的胶原纤维和弹力纤维,内弹力板下方以收缩型平滑肌为主.结论 TS7组大鼠胸主动脉和肺动脉出现损伤和增殖并存,以肺动脉较明显;TS14组肺动脉趋于形成新的稳定结构,而胸主动脉新稳定结构还未形成.模拟微重力时大小循环血管发生了结构重塑,大小循环血管重塑的时间过程不同归因于模拟微重力初期由下体转移而来的体液进入大小循环高峰期的时间差.     

血管内皮细胞功能检测方法的研究进展

血管内皮细胞(VEC)是多种心脑血管疾病或危险因子作用的靶器官,内皮功能损伤常伴发和加重心脑血管疾病,血管内皮功能障碍与动脉粥样硬化、高血压等一系列疾病和状态有关,是动脉粥样硬化最早期的改变,是冠心病患者未来心血管事件增加的一项独立的预测指标.如何早期评价血管内皮的功能对于临床防治血管性疾病具有重要意义.目前临床检测方法主要包括影像学检查、生物活性因子检测及循环内皮细胞和内皮祖细胞计数.     

淋巴管内皮细胞的生物学特性

淋巴管作为机体内流体动力学系统之一 ,对于维持组织液的平衡、淋巴细胞的再循环 ( Recirculation of lymphocyte)、蛋白质等大分子物质的转运 ,都具有非常重要的作用。近年来研究表明 :淋巴管内皮细胞具有活跃的代谢功能 ,能够生成和灭活多种生物活性物质。本文对近年来淋巴管内皮细胞的生物学特性研究综述如下。1　淋巴管内皮细胞的生物学特性1.1　血管紧张素的转化淋巴管内皮细胞中含有 A型血管紧张素 转移酶。血管紧张素转移酶分布于内皮细胞的表面 ,已被广泛用作内皮细胞的标志。血管紧张素 转移酶是一种羧基肽酶 ,能将十肽的血管紧…     

血管内皮生长因子在风湿病中的研究进展

血管内皮生长因子(vascular endothelial growth factor,VEGF)又叫血管渗透因子(vascular permeability factor,VPF)是一种特异性的促进血管内皮细胞增殖、维持血管内皮细胞分化状态、提高微血管通透性的细胞因子。作为血管新生需要诱导剂的VEGF,其与风湿病的关系近年来备受关注。本就VEGF生物学特性及其与风湿病的研究进展作一综述。     

尾部悬吊大鼠胸主动脉、肺动脉超微结构变化的动态观察

目的观察模拟微重力时大小循环动脉血管超微结构重塑随时间变化的差异,为微重力后立位耐力降低的机制研究积累资料。方法用透射电镜观察-30°尾部悬吊7d(TS7组)、14d(TS14组)及对照组大鼠胸主动脉、肺动脉壁超微结构的变化。结果TS7组胸主动脉内皮细胞表面出现绒毛状突起,部分线粒体空泡变性,内皮下基膜有分层,内弹力板较厚,且厚度不均匀,内弹力板下出现大量的胶原纤维;TS14组胸主动脉内皮细胞变性较明显,部分内皮细胞基质致密化,基膜复层化,内弹力板有破碎,弹力纤维增多。TS7组肺动脉部分内皮细胞突起,细胞内出现脂滴,内皮细胞基膜出现分层状改变,弹力板变薄、断裂,其下方可见收缩型平滑肌及合成型平滑肌细胞;TS14组肺动脉内皮细胞空泡变性较明显,内弹力板未见明显改变,弹力板内外均可见较多的胶原纤维和弹力纤维,内弹力板下方以收缩型平滑肌为主。结论TS7组大鼠胸主动脉和肺动脉出现损伤和增殖并存,以肺动脉较明显;TS14组肺动脉趋于形成新的稳定结构,而胸主动脉新稳定结构还未形成。模拟微重力时大小循环血管发生了结构重塑,大小循环血管重塑的时间过程不同归因于模拟微重力初期由下体转移而来的体液进入大小循环高峰期的时间差。     

Impact of simulated microgravity on microvascular endothelial cell apoptosis

Cardiovascular deconditioning is known to occur in astronauts exposed to microgravity. Endothelial dysfunction at microcirculatory sites might contribute to cardiovascular deconditioning induced by weightlessness. Recent studies have reported changes in the morphology and gene expression of endothelial cells exposed to conditions of simulated microgravity. The present study was aimed at examining the effects of microgravity on the apoptosis of microvascular endothelial cells and the mechanism underlying these effects. We simulated a microgravity environment and found that microgravity induced microvascular endothelial cell apoptosis and that this effect was correlated with the downregulation of the PI3K/Akt pathway, increased expression of NF-κB, and depolymerization of F-actin. These findings may provide important insights into the origin of the adverse physiological changes occurring due to exposure to microgravity conditions.     

Are energy metabolism alterations involved in cardiovascular deconditioning after weightlessness? An hypothesis

The physiopathogenesis of the cardiovascular deconditioning syndrome observed after actual and simulated microgravity is still under debate, despite numerous studies conducted on the role of blood volume, hormones involved in its regulation, sympathetic nervous system, baroreflexes and venous compliance. Orthostatic intolerance, a reduced exercise capacity and an increased heart rate at rest characterize this syndrome. Recent data suggest, first, the presence of a complex loop between the sympathetic nervous system, carbohydrate metabolism (insulin) and leptin hormone and, second, that this loop, an overall reflection of energy metabolism, participates in cardiovascular regulation. After a resume of studies conducted on fuel homeostasis during actual and simulated microgravity, the possible implications of energy metabolism in the development of the cardiovascular deconditioning syndrome will be discussed.     

Preserved contribution of nitric oxide to baseline vascular tone in deconditioned human skeletal muscle

Deconditioning is a risk factor for cardiovascular disease. Exercise reduces this risk, possibly by improving the vascular endothelial nitric oxide (NO) pathway. The effect of deconditioning on the NO pathway is largely unknown. This study was designed to assess baseline NO availability in the leg vascular bed after extreme, long-term deconditioning (spinal cord-injured individuals, SCI) as well as after moderate, short-term deconditioning (4 weeks of unilateral lower limb suspension, ULLS). For this purpose, seven SCI were compared with seven matched controls. Additionally, seven healthy subjects were studied pre- and post-ULLS. Leg blood flow was measured by venous occlusion plethysmography at baseline and during infusion of 5 incremental dosages of N ^G-monomethyl- l -arginine ( l -NMMA) into the femoral artery. Sodium nitroprusside (SNP) was infused to test vascular responsiveness to NO. Baseline leg vascular resistance tended to be higher in SCI compared with controls (37 ± 4 versus 31 ± 2 arbitrary units (AU), P = 0.06). Deconditioning altered neither the vasoconstrictor response to l -NMMA (increase in resistance in SCI versus controls: 102 ± 33% versus 69 ± 9%; pre- versus post-ULLS: 95 ± 18% versus 119 ± 15%), nor the vascular responsiveness to NO. In conclusion, two human in vivo models of deconditioning show a preserved baseline NO availability in the leg skeletal muscle vascular bed.     

Impact of inactivity and exercise on the vasculature in humans

The effects of inactivity and exercise training on established and novel cardiovascular risk factors are relatively modest and do not account for the impact of inactivity and exercise on vascular risk. We examine evidence that inactivity and exercise have direct effects on both vasculature function and structure in humans. Physical deconditioning is associated with enhanced vasoconstrictor tone and has profound and rapid effects on arterial remodelling in both large and smaller arteries. Evidence for an effect of deconditioning on vasodilator function is less consistent. Studies of the impact of exercise training suggest that both functional and structural remodelling adaptations occur and that the magnitude and time-course of these changes depends upon training duration and intensity and the vessel beds involved. Inactivity and exercise have direct “vascular deconditioning and conditioning” effects which likely modify cardiovascular risk.     

内皮祖细胞在肺动脉高压中的研究进展

肺动脉高压(pulmonary hypertension,PH)是指在海平面静息状态下平均肺动脉压(mean pulmonary arterial pressure,mPAP)≥20 mmHg,肺血管阻力(pulmonary vascular resistance,PVR)≥3 Wood units的一种疾病或病理生理综合征^[1]。PH的病理特征主要是肺小血管结构和血管壁细胞功能变化导致的肺血管重塑,从而引起肺血管阻力增加,进而导致右心功能下降乃至右心衰竭,最后患者死亡^[2]。     

内皮祖细胞与雌激素

背景：研究发现雌激素对血管内皮具有明显的保护作用,而内皮祖细胞作为内皮细胞的前体细胞参与内皮的修复。 目的：总结内皮祖细胞生物特点及雌激素对内皮祖细胞作用的研究进展。 方法：应用计算机检索PubMed数据库及CNKI数据库,在标题和摘要中以“内皮祖细胞,雌激素”或“Endothelial progenitor cells,estrogen”为检索词进行检索。选择与内皮祖细胞生物学特点及雌激素对其作用研究相关的文献。 结果与结论：内皮祖细胞存在于骨髓和外周血中,是具有增殖、迁移、黏附能力并分化为血管内皮细胞潜能的原始细胞,可作为未来治疗心血管疾病的重要的靶点。雌激素对内皮祖细胞有保护效应,能增强内皮祖细胞增殖、迁移、黏附等生物活性,同时还能延迟内皮祖细胞衰老、拮抗其凋亡。但雌激素影响内皮祖细胞生物活性的具体靶点及机制尚有待进一步研究。     

血管内皮细胞迁移及相关影响因素研究进展

内皮细胞迁移功能在血管新生、伤口愈合、内皮损伤的愈合等过程中起着重要的作用。此外,在部分心血管疾病中尤其在动脉粥样硬化发生的某些阶段中,内皮细胞的迁移特性也起着重要的作用。因此了解内皮细胞迁移特性及相关的影响因素对于掌握内皮细胞在这些生理和病理过程中的作用有着重要的意义。重点就目前内皮细胞迁移的诱导、抑制因素以及血流、细胞骨架和胞外基质对内皮细胞迁移的影响的研究进展做了较为详细的介绍,并着重讨论了在动脉粥样硬化的发展过程中,血管内皮细胞脱落区的修复、动脉粥样硬化斑块内的血管新生等与内皮细胞迁移特性之间的紧密联系。     

Space physiology VI: exercise, artificial gravity, and countermeasure development for prolonged space flight

When applied individually, exercise countermeasures employed to date do not fully protect the cardiovascular and musculoskeletal systems during prolonged spaceflight. Recent ground-based research suggests that it is necessary to perform exercise countermeasures within some form of artificial gravity to prevent microgravity deconditioning. In this regard, it is important to provide normal foot-ward loading and intravascular hydrostatic-pressure gradients to maintain musculoskeletal and cardiovascular function. Aerobic exercise within a centrifuge restores cardiovascular function, while aerobic exercise within lower body negative pressure restores cardiovascular function and helps protect the musculoskeletal system. Resistive exercise with vibration stimulation may increase the effectiveness of resistive exercise by preserving muscle function, allowing lower intensity exercises, and possibly reducing risk of loss of vision during prolonged spaceflight. Inexpensive methods to induce artificial gravity alone (to counteract head-ward fluid shifts) and exercise during artificial gravity (for example, by short-arm centrifuge or exercise within lower body negative pressure) should be developed further and evaluated as multi-system countermeasures.