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宫内生长受限胎儿羊的动脉僵硬度增加和细胞外基质重构。

Increased arterial stiffness and extracellular matrix reorganization in intrauterine growth-restricted fetal sheep.

机构信息

Department of Mechanical Engineering, University of Colorado at Boulder, Boulder, Colorado, USA.

出版信息

Pediatr Res. 2013 Feb;73(2):147-54. doi: 10.1038/pr.2012.156. Epub 2012 Nov 15.

DOI:10.1038/pr.2012.156
PMID:23154756
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3742323/
Abstract

BACKGROUND

Fetal intrauterine growth restriction (IUGR) results in increased placental resistance to blood flow, fetal hypertension, and increased pulsatility stresses shown to lead to vascular remodeling. We tested our hypothesis that IUGR causes decreased compliance in the carotid and umbilical arteries due to altered extracellular matrix (ECM) composition and structure.

METHODS

A sheep model of placental insufficiency-induced IUGR (PI-IUGR) was created by exposure of the pregnant ewe to elevated ambient temperatures. Umbilical and carotid arteries from near-term fetuses were tested with pressure-diameter measurements to compare passive compliance in control and PI-IUGR tissues. ECM composition was measured via biochemical assay, and the organization was determined by using histology and second-harmonic generation imaging.

RESULTS

We found that PI-IUGR increased arterial stiffness with increased collagen engagement, or transition stretch. PI-IUGR carotid arteries exhibited increased collagen and elastin quantity, and PI-IUGR umbilical arteries exhibited increased sulfated glycosaminoglycans. Histomorphology showed altered collagen-to-elastin ratios with altered cellular proliferation. Increased stiffness indicates altered collagen-to-elastin ratios with less elastin contribution leading to increased collagen engagement.

CONCLUSION

Because vessel stiffness is a significant predictor in the development of hypertension, disrupted ECM deposition in IUGR provides a potential link between IUGR and adult hypertension.

摘要

背景

胎儿宫内生长受限（IUGR）导致胎盘对血流的阻力增加、胎儿高血压和脉动压力增加，这些都会导致血管重塑。我们验证了我们的假设，即 IUGR 通过改变细胞外基质（ECM）的组成和结构导致颈动脉和脐带动脉顺应性降低。

方法

通过将妊娠母羊暴露在升高的环境温度下来创建胎盘功能不全引起的宫内生长受限（PI-IUGR）绵羊模型。通过压力-直径测量来比较对照组和 PI-IUGR 组织中的被动顺应性，从而测试来自近足月胎儿的脐动脉和颈动脉。通过生化测定测量 ECM 组成，通过组织学和二次谐波产生成像来确定组织的结构。

结果

我们发现，PI-IUGR 增加了动脉僵硬度，增加了胶原蛋白的参与或过渡拉伸。PI-IUGR 颈动脉表现出增加的胶原蛋白和弹性蛋白数量，而 PI-IUGR 脐动脉表现出增加的硫酸化糖胺聚糖。组织形态学显示胶原蛋白与弹性蛋白比值的改变，伴有细胞增殖的改变。僵硬度的增加表明胶原蛋白与弹性蛋白比值的改变，弹性蛋白的贡献减少导致胶原蛋白的参与增加。

结论

由于血管僵硬度是高血压发展的重要预测因素，因此 IUGR 中 ECM 沉积的破坏为 IUGR 与成人高血压之间提供了潜在联系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8820/3742323/48c29ab61cf1/nihms480255f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8820/3742323/c07d410c420c/nihms480255f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8820/3742323/16ff389ab83a/nihms480255f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8820/3742323/3973a6f6c857/nihms480255f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8820/3742323/68ff67c42d82/nihms480255f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8820/3742323/48c29ab61cf1/nihms480255f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8820/3742323/c07d410c420c/nihms480255f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8820/3742323/16ff389ab83a/nihms480255f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8820/3742323/3973a6f6c857/nihms480255f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8820/3742323/68ff67c42d82/nihms480255f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8820/3742323/48c29ab61cf1/nihms480255f5.jpg

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