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Regulation of the human coronary microcirculation.人冠状动脉微循环的调节。
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本文引用的文献

1
NADPH oxidases in cardiovascular disease: insights from in vivo models and clinical studies.还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶在心血管疾病中的作用:来自体内模型和临床研究的新见解。
Basic Res Cardiol. 2011 Sep;106(5):735-47. doi: 10.1007/s00395-011-0190-z. Epub 2011 May 20.
2
Role of endothelial Nox2 NADPH oxidase in angiotensin II-induced hypertension and vasomotor dysfunction.内皮型 Nox2 NADPH 氧化酶在血管紧张素Ⅱ诱导的高血压和血管舒缩功能障碍中的作用。
Basic Res Cardiol. 2011 Jun;106(4):527-38. doi: 10.1007/s00395-011-0179-7. Epub 2011 Apr 29.
3
Arterial flow reduces oxidative stress via an antioxidant response element and Oct-1 binding site within the NADPH oxidase 4 promoter in endothelial cells.动脉血流通过内皮细胞中 NADPH 氧化酶 4 启动子中的抗氧化反应元件和 Oct-1 结合位点减少氧化应激。
Basic Res Cardiol. 2011 Jun;106(4):551-61. doi: 10.1007/s00395-011-0170-3. Epub 2011 Mar 12.
4
Mitochondrial complex I and NAD(P)H oxidase are major sources of exacerbated oxidative stress in pressure-overloaded ischemic-reperfused hearts.线粒体复合物 I 和 NAD(P)H 氧化酶是压力超负荷缺血再灌注心脏中氧化应激加剧的主要来源。
Basic Res Cardiol. 2011 Mar;106(2):287-97. doi: 10.1007/s00395-011-0150-7. Epub 2011 Jan 19.
5
H2O2 is the transferrable factor mediating flow-induced dilation in human coronary arterioles.H2O2 是介导人冠状动脉小动脉血流诱导扩张的可传递因子。
Circ Res. 2011 Mar 4;108(5):566-73. doi: 10.1161/CIRCRESAHA.110.237636. Epub 2011 Jan 13.
6
Effect of PAR2 in regulating TNF-α and NAD(P)H oxidase in coronary arterioles in type 2 diabetic mice.PAR2 在调节 2 型糖尿病小鼠冠状动脉小动脉中 TNF-α 和 NAD(P)H 氧化酶中的作用。
Basic Res Cardiol. 2011 Jan;106(1):111-23. doi: 10.1007/s00395-010-0129-9. Epub 2010 Oct 24.
7
Functional role of vanilloid transient receptor potential 4-canonical transient receptor potential 1 complex in flow-induced Ca2+ influx.香草素瞬时受体电位 4-经典瞬时受体电位 1 复合物在流动诱导的 Ca2+内流中的功能作用。
Arterioscler Thromb Vasc Biol. 2010 Apr;30(4):851-8. doi: 10.1161/ATVBAHA.109.196584. Epub 2010 Jan 21.
8
Signaling functions of reactive oxygen species.活性氧的信号转导功能。
Biochemistry. 2010 Feb 9;49(5):835-42. doi: 10.1021/bi9020378.
9
TRPV4-mediated endothelial Ca2+ influx and vasodilation in response to shear stress.机械切应力刺激诱导的 TRPV4 介导的内皮细胞钙离子内流和血管舒张。
Am J Physiol Heart Circ Physiol. 2010 Feb;298(2):H466-76. doi: 10.1152/ajpheart.00854.2009. Epub 2009 Dec 4.
10
Adenosine and maximum coronary vasodilation in humans: myth and misconceptions in the assessment of coronary reserve.腺苷与人类冠状动脉最大舒张:冠状动脉储备评估中的误区与误解
Basic Res Cardiol. 2010 Jan;105(1):1-5. doi: 10.1007/s00395-009-0074-7.

人冠状动脉微循环的调节。

Regulation of the human coronary microcirculation.

机构信息

Department of Medicine, Cardiology Division Medical College of Wisconsin, Milwaukee, WI 53226, United States.

出版信息

J Mol Cell Cardiol. 2012 Apr;52(4):814-21. doi: 10.1016/j.yjmcc.2011.10.003. Epub 2011 Oct 12.

DOI:10.1016/j.yjmcc.2011.10.003
PMID:22033434
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3306504/
Abstract

Atherosclerosis of conduit epicardial arteries is the principal culprit behind the complications of coronary heart disease, but a growing body of literature indicates that the coronary microcirculation also contributes substantially to the pathophysiology of cardiovascular disease. An understanding of mechanisms regulating microvascular function in humans is an essential foundation for understanding the role in disease, especially since these regulatory mechanisms vary substantially across species and vascular beds. In fact all subjects whose coronary tissue was used in the studies described have medical conditions that warrant cardiac surgery, thus relevance to the normal human must be inferential and is based on tissue from subjects without known arteriosclerotic disease. This review will focus on recent advances in the physiological and pathological mechanisms of coronary microcirculatory control, describing a robust plasticity in maintaining endothelial control over dilation, including mechanisms that are most relevant to the human heart. This article is part of a Special Issue entitled "Coronary Blood Flow".

摘要

心外膜大冠状动脉粥样硬化是冠心病并发症的主要罪魁祸首,但越来越多的文献表明,冠状动脉微循环也对心血管疾病的病理生理学有重要贡献。了解调节人类微血管功能的机制是理解其在疾病中的作用的重要基础,特别是因为这些调节机制在物种和血管床之间有很大的差异。事实上,所有在描述的研究中使用过冠状动脉组织的对象都有需要心脏手术的医疗条件,因此与正常人类的相关性必须是推断性的,并且是基于没有已知动脉粥样硬化疾病的对象的组织。这篇综述将集中讨论冠状动脉微循环控制的生理和病理机制的最新进展,描述了维持内皮细胞对扩张控制的强大可塑性,包括与人类心脏最相关的机制。本文是一个题为“冠状动脉血流”的特刊的一部分。