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尽管猪的重复性压力超负荷已停止,但仍存在持续性纤维化和左心室腔硬化。

Persistent Fibrosis and Left Ventricular Chamber Stiffening Despite Cessation of Repetitive Pressure Overload in Swine.

作者信息

Weil Brian R, Graser Luke, Rasam Sailee, Zimmer Henry, Konecny Filip, Techiryan George, Starling Charlotte, Qu Jun, Canty John M

机构信息

VA WNY Health Care System, Buffalo, New York, USA; Department of Physiology & Biophysics, University at Buffalo, Buffalo, New York, USA; Clinical and Translational Research Center of the University at Buffalo, Buffalo, New York, USA.

Department of Pharmacology & Toxicology, University at Buffalo, Buffalo, New York, USA.

出版信息

JACC Basic Transl Sci. 2025 Jun;10(6):844-859. doi: 10.1016/j.jacbts.2025.02.009. Epub 2025 Apr 30.

DOI:10.1016/j.jacbts.2025.02.009
PMID:40562497
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12230478/
Abstract

To determine whether repetitive pressure overload-induced left ventricular (LV) fibrosis and LV chamber stiffening are reversible upon normalization of hemodynamics, swine were subjected to 2 weeks of daily phenylephrine (2 h/d) followed by a 2-week or 4-week recovery period. Despite cessation of repetitive pressure overload, interstitial fibrosis persisted, and LV chamber stiffness remained increased for up to 4 weeks of recovery. The persistent increase in LV chamber stiffness was accompanied by dynamic changes in extracellular matrix protein expression. The rapid and persistent increase in LV chamber stiffness may explain how hypertrophy-independent LV stiffening develops in the absence of sustained hypertension.

摘要

为了确定重复性压力超负荷诱导的左心室(LV)纤维化和左心室腔僵硬度在血流动力学恢复正常后是否可逆,对猪每日给予去氧肾上腺素2周(每天2小时),随后进行2周或4周的恢复期。尽管重复性压力超负荷停止,但间质纤维化持续存在,并且左心室腔僵硬度在长达4周的恢复期内仍保持增加。左心室腔僵硬度的持续增加伴随着细胞外基质蛋白表达的动态变化。左心室腔僵硬度的快速和持续增加可能解释了在没有持续性高血压的情况下非肥厚性左心室僵硬度是如何发展的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/def47427d262/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/7a8cbc895134/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/b39203cc4743/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/d0c5af470ead/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/296bcd56ee6f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/f3d30a4e6854/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/def47427d262/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/7a8cbc895134/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/b39203cc4743/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/d0c5af470ead/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/296bcd56ee6f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/f3d30a4e6854/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a578/12230478/def47427d262/gr6.jpg

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Left Ventricular Gene Expression in Heart Failure With Preserved Ejection Fraction-Profibrotic and Proinflammatory Pathways and Genes.左心室射血分数保留心力衰竭的基因表达——成纤维细胞增生和炎症途径及基因。
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