共查询到18条相似文献,搜索用时 93 毫秒
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肺动脉高压是以血管增殖重塑、原位血栓形成、肺血管床进行性闭塞、肺血管阻力进行性增高为特征的肺小动脉疾病。其发病机制是一个复杂的、多因素参与的过程。近来越来越多的研究表明,肺脏血管内皮功能障碍在肺动脉高压形成的起始及发展阶段都起着重要作用。正常的肺脏血管内皮衬于肺血管内腔表面,介于循环血和肺血管平滑肌之间。其不仅具有生理屏障功能,还有调解血管张力,血液流动性和黏附性,参与血管内皮损伤的修复,同时血管内皮可以通过膜受体感知血流动力学和血源性信号变化参与细胞间的信号传导[1]。肺脏内皮功能障碍是肺脏内皮细胞在… 相似文献
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血管内皮生长因子是作用于血管内皮细胞的重要血管调节因子,它通过与内皮上的特异受体结合,发挥促进内皮细胞增殖、分化、诱导血管生成、增加微血管通透性等多种功能。近年研究显示血管内皮生长因子在慢性阻塞性肺疾病、肺动脉高压、急性肺损伤、肺癌等疾病发病中起到了重要作用。本文就血管内皮生长因子在慢性阻塞性肺疾病、肺动脉高压、急性肺损伤、肺癌等疾病中的作用综述如下。 相似文献
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慢性缺氧性肺动脉高压大鼠内皮依赖性舒缩因子的变化 总被引:5,自引:0,他引:5
慢性缺氧性肺动脉高压大鼠内皮依赖性舒缩因子的变化李志斌邹霞英容中生缺氧性肺血管收缩反应(HPV)和肺血管结构重建是缺氧性肺动脉高压(PH)形成和发展的主要因素。缺氧致肺血管内皮细胞(EC)损伤[1],影响EC分泌内皮依赖性舒缩因子的平衡,增强HPV和... 相似文献
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血管内皮生长因子(vascular endothelial growth factor,VEGF)是一种重要的血管内皮细胞丝裂原和通透因子.肺血管的重塑与慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)继发肺动脉高压密切相关.VEGF贯穿于COPD发展的全过程,在COPD的不同时期呈现不同的表达水平,发挥不同的生物学作用.气道炎症、低氧等因素可以在COPD早期促进VEGF及其受体的表达上调从而导致肺血管重塑的发生发展,VEGF也可以对COPD后期继发肺动脉高压时的重度肺血管重塑起到一定的修复作用.通过阐述VEGF、COPD肺血管重塑及继发肺动脉高压之间的相互关系,可以对COPD继发肺动脉高压的诊断和治疗提供新的思路. 相似文献
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随着肺动脉高压研究的不断深入,肺血管内皮细胞凋亡在肺动脉高压形成过程中的重要作用被逐步认识。多种疾病和环境因素导致肺血管内皮损伤、内皮细胞凋亡增加、功能障碍,从而促进肺动脉平滑肌细胞和成纤维细胞增殖、肺动脉重构和血栓形成;肺血管内皮细胞凋亡还诱导产生凋亡抵抗表型的内皮细胞过度增殖,形成丛样病变和肺血管闭塞,最终导致严重肺动脉高压。因而在肺动脉高压发生发展的不同时期,调控肺血管内皮细胞凋亡可能是预防和治疗肺动脉高压的一种新策略。 相似文献
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氧化应激可通过促进肺动脉血管平滑肌细胞增殖、加重血管内皮功能损伤和促进血管外基质增生等多条途径参与肺动脉血管重构,加速肺动脉高压的发生发展进程。近来研究发现,针对氧化应激进行的抗氧化治疗可有效地抑制肺动脉血管重构及肺动脉高压的发生,进一步证明了氧化应激在肺动脉血管重构乃至肺动脉高压中的重要作用。阐明病理条件下氧化还原信号途径,寻找抗氧化治疗的特异性药物,是肺动脉高压抗氧化治疗的基础和研究方向。 相似文献
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Morgan E. Whitaker Vineet Nair Shripad Sinari Parinita A. Dherange Balaji Natarajan Lindsey Trutter Evan L. Brittain Anna R. Hemnes Eric D. Austin Kumar Patel Stephen M. Black Joe G.N. Garcia Jason X. Yuan MD PhD Rebecca R. Vanderpool Franz Rischard Ayako Makino Edward J. Bedrick Ankit A. Desai 《The American journal of medicine》2018,131(6):702.e7-702.e13
Background
Diabetes mellitus is associated with left ventricular hypertrophy and dysfunction. Parallel studies have also reported associations between diabetes mellitus and right ventricular dysfunction and reduced survival in patients with pulmonary arterial hypertension. However, the impact of diabetes mellitus on the pulmonary vasculature has not been well characterized. We hypothesized that diabetes mellitus and hyperglycemia could specifically influence right ventricular afterload and remodeling in patients with Group I pulmonary arterial hypertension, providing a link to their known susceptibility to right ventricular dysfunction.Methods
Using an adjusted model for age, sex, pulmonary vascular resistance, and medication use, associations of fasting blood glucose, glycated hemoglobin, and the presence of diabetes mellitus were evaluated with markers of disease severity in 162 patients with pulmonary arterial hypertension.Results
A surrogate measure of increased pulmonary artery stiffness, elevated pulmonary arterial elastance (P = .012), along with reduced log(pulmonary artery capacitance) (P = .006) were significantly associated with the presence of diabetes mellitus in patients with pulmonary arterial hypertension in a fully adjusted model. Similar associations between pulmonary arterial elastance and capacitance were noted with both fasting blood glucose and glycated hemoglobin. Furthermore, right ventricular wall thickness on echocardiography was greater in pulmonary arterial hypertension patients with diabetes, supporting the link between right ventricular remodeling and diabetes.Conclusion
Cumulatively, these data demonstrate that an increase in right ventricular afterload, beyond pulmonary vascular resistance alone, may influence right ventricular remodeling and provide a mechanistic link between the susceptibility to right ventricular dysfunction in patients with both diabetes mellitus and pulmonary arterial hypertension. 相似文献14.
慢性阻塞性肺疾病合并肺动脉高压的发病机制研究进展 总被引:2,自引:0,他引:2
肺动脉高压(pulmonary hypertension,PH)是慢性阻塞性肺疾病(chronic obstructivepulmonary disease,COPD)的一个重要合并症.COPD合并PH是逐渐发生和进展的,最初于运动或睡眠时出现,逐渐发展为休息时即存在PH,运动、睡眠或病情恶化时进一步升高.COPD相关的PH多为轻到中度,但某些COPD患者可表现为"不成比例"的PH.香烟烟雾、炎症产物引起内皮损害,造成内皮功能失调;慢性低氧引起肺血管收缩;肺血管重构导致管腔变小,血管膨胀性降低,阻力增加;重度肺气肿时肺毛细血管的丧失等均与COPD时的PH相关. 相似文献
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Rajamma Mathew Jing Huang Joseph M Wu John T Fallon Michael H Gewitz 《World journal of cardiology》2016,8(12):703-718
Pulmonary hypertension(PH),a serious disorder with a high morbidity and mortality rate,is known to occur in a number of unrelated systemic diseases.Several hematological disorders such as sickle cell disease,thalassemia and myeloproliferative diseases develop PH which worsens the prognosis.Associated oxidant injury and vascular inflammation cause endothelial damage and dysfunction.Pulmonary vascular endothelial damage/dysfunction is an early event in PH resulting in the loss of vascular reactivity,activation of proliferative and antiapoptotic pathways leading to vascular remodeling,elevated pulmonary artery pressure,right ventricular hypertrophy and premature death.Hemolysis observed in hematological disorders leads to free hemoglobin which rapidly scavenges nitric oxide(NO),limiting its bioavailability,and leading to endothelial dysfunction.In addition,hemolysis releases arginase into the circulation which converts L-arginine to ornithine,thus bypassing NO production.Furthermore,treatments for hematological disorders such as immunosuppressive therapy,splenectomy,bone marrow transplantation,and radiation have been shown to contribute to the development of PH.Recent studies have shown deregulated iron homeostasis in patients with cardiopulmonary diseases including pulmonary arterial hypertension(PAH).Several studies have reported low iron levels in patients with idiopathic PAH,and iron deficiency is an important risk factor.This article reviews PH associated with hematological disorders and its mechanism:and iron homeostasis and its relevance to PH. 相似文献
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Bahri Akdeniz 《老年心脏病学杂志》2017,14(1):28-34
In recent times, the prevalence of pulmonary arterial hypertension (PAH) is more commonly seen among elderly populations. The increased prevalence of hypertension, diabetes, obesity, arterial stiffness, as well as diastolic dysfunction, may cause endothelial dysfunction and affect pulmonary vasculature. Furthermore, older patients have certain differences in clinical characteristics and outcomes. In this article, the special characteristics of aging in PAH patients have been reviewed, while the risk predictors of elderly patients are also discussed. 相似文献
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目的:探讨肺动脉高压(pulmonary hypertension,PH)患者血浆肾上腺髓质素(a-drenomedullin,AM)的浓度与肺动脉压力的关系。方法:选择正常肺动脉压力患者和轻度、中度、重度肺动脉高压患者各10例,在术中分别从肺动脉和肺静脉中抽血用放射免疫法测定AM含量。结果:肺动脉血浆AM浓度与肺动脉压力呈显著正相关;肺静脉血浆AM浓度低于肺动脉AM浓度,且其浓度差值与肺动脉压力呈显著正相关。结论:AM参与了肺动脉高压的病理生理过程,并在肺内部分代谢,对肺血管张力的调节起重要作用。 相似文献
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Altered endothelial function in lambs with pulmonary hypertension and acute lung injury 总被引:2,自引:0,他引:2
Fineman JR Wong J Mikhailov T Vanderford PA Jerome HE Soifer SJ 《Pediatric pulmonology》1999,27(3):147-156
Acute lung injury produces pulmonary hypertension, altered vascular reactivity, and endothelial injury. To determine whether acute lung injury impairs the endothelium-dependent regulation of pulmonary vascular tone, 16 lambs were studied during U46619-induced pulmonary hypertension without acute lung injury, or air embolization-induced pulmonary hypertension with acute lung injury. The hemodynamic responses to endothelium-dependent (acetylcholine, ATP, ET-1, and 4 Ala ET-1 [an ETb receptor agonist]) and endothelium-independent (nitroprusside and isoproterenol) vasodilators were compared. During U46619-induced pulmonary hypertension, all vasodilators decreased pulmonary arterial pressure and vascular resistance (P < 0.05). During air embolization-induced pulmonary hypertension, the pulmonary vasodilating effects of acetylcholine, ATP, and 4 Ala ET-1 were attenuated (P < 0.05); the pulmonary vasodilating effects of nitroprusside and isoproterenol were unchanged; and the pulmonary vasodilating effects of ET-1 were reversed, producing pulmonary vasoconstriction (P < 0.05). During air embolization, the pulmonary vasoconstricting effects of ET-1 were blocked by BQ 123, an ETa receptor antagonist. The systemic effects of the vasoactive drugs were similar during both conditions. We conclude that pulmonary hypertension with acute lung injury induced by air embolization results in endothelial dysfunction; there is selective impairment of endothelium-dependent pulmonary vasodilation and an altered response to ET-1 from pulmonary vasodilation to vasoconstriction. This altered response to ET-1 is associated with decreased ETb receptor-mediated vasodilation and increased ETa receptor-mediated vasoconstriction. Endothelial injury and dysfunction account, in part, for the altered regulation of pulmonary vascular tone during pulmonary hypertension with acute lung injury. 相似文献