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跨壁压力和轴向负荷在体外交互调节动脉重塑。

Transmural pressure and axial loading interactively regulate arterial remodeling ex vivo.

作者信息

Lawrence Amanda R, Gooch Keith J

机构信息

Department of Bioengineering and Institute for Medicine and Engineering, University of Pennsylvania, Philadelphia, PA, USA.

出版信息

Am J Physiol Heart Circ Physiol. 2009 Jul;297(1):H475-84. doi: 10.1152/ajpheart.00972.2008. Epub 2009 May 22.

DOI:10.1152/ajpheart.00972.2008
PMID:19465545
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2711737/
Abstract

Physiological axial strains range between 40 and 60% in arteries, resulting in stresses comparable to those due to normal blood pressure or flow. To investigate the contribution of axial strain to arterial remodeling and function, porcine carotid arteries were cultured for 9 days at physiological and reduced axial stretch ratios in the presence of normotensive and hypertensive transmural pressures by ex vivo perfusion techniques. Consistent with previous in vivo studies, vessels cultured with physiological levels of axial strain and exposed to hypertensive pressure had greater mass, wall area, and outer diameter relative to those cultured at the same axial stretch ratio and normotensive pressure. Reducing the amount of axial strain resulted in mass loss and decreased cell proliferation. Culture in a hypertensive pressure environment at reduced axial strain produced arteries with greater contractility in response to norepinephrine. Arteries cultured at reduced axial strain with the matrix metalloproteinase inhibitor GM6001 maintained their masses over culture, indicating a possible mechanism for this model of axial stretch-dependent remodeling. Although not historically considered one of the primary stimuli for remodeling, multiple linear regression analysis revealed that axial strain had an impact similar to or greater than transmural pressure on various remodeling indexes (i.e., outer diameter, wall area, and wet mass), suggesting that axial strain is a primary mediator of vascular remodeling.

摘要

动脉中的生理轴向应变范围在40%至60%之间,所产生的应力与正常血压或血流所产生的应力相当。为了研究轴向应变对动脉重塑和功能的作用,采用体外灌注技术,将猪颈动脉在生理和降低的轴向拉伸率下,于正常血压和高血压跨壁压力条件下培养9天。与先前的体内研究一致,与在相同轴向拉伸率和正常血压条件下培养的血管相比,在生理水平的轴向应变下培养并暴露于高血压压力的血管具有更大的质量、壁面积和外径。减少轴向应变的量会导致质量损失和细胞增殖减少。在降低的轴向应变下于高血压压力环境中培养的动脉对去甲肾上腺素的反应具有更大的收缩性。在降低的轴向应变下用基质金属蛋白酶抑制剂GM6001培养的动脉在培养过程中保持了它们的质量,这表明了这种轴向拉伸依赖性重塑模型的一种可能机制。尽管轴向应变在历史上并不被认为是重塑的主要刺激因素之一,但多元线性回归分析显示,轴向应变对各种重塑指标(即外径、壁面积和湿质量)的影响与跨壁压力相似或更大,这表明轴向应变是血管重塑的主要介质。

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本文引用的文献

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