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一种新型的减阻聚合物水动力方法,用于改善自发性高血压大鼠的左心室肥厚和主动脉重塑。

A novel hydrodynamic approach of drag-reducing polymers to improve left ventricular hypertrophy and aortic remodeling in spontaneously hypertensive rats.

机构信息

Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou.

The Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Sciences of Ministry of Education, Peking University Health Science Center.

出版信息

Int J Nanomedicine. 2016 Dec 13;11:6743-6751. doi: 10.2147/IJN.S119607. eCollection 2016.

DOI:10.2147/IJN.S119607
PMID:28008249
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5167458/
Abstract

Drag-reducing polymers (DRPs), when added in minute concentrations, have been shown to decrease peripheral vascular resistance. In this study, the effect of DRPs on the hypertension-induced left ventricular hypertrophy and aortic remodeling was evaluated in spontaneously hypertensive rats (SHR). Male SHR and age-matched Wistar rats were divided into four groups and received intravenous injection of normal saline (NS) or DRPs. Body weight (BW), heart rate (HR) and systolic blood pressure (SBP) were measured. Echocardiography was used to evaluate the changes in left ventricle (LV) function and global wall motion. The LV and aorta were stained by hematoxylin and eosin. Cell size of cardiomyocytes and aortic medial thickness were evaluated for each section. The expression of endothelin-1 (ET-1) of LV and aorta was examined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunohistochemistry. There was no significant difference in the increase of SBP among SHR + NS, SHR + 10DRP and SHR + 20DRP groups. SHR + NS group had markedly smaller left ventricular end-systolic diameter and left ventricular end-diastolic diameter but bigger anterior and posterior systolic wall thicknesses, while there was no significant difference in fractional shortening and ejection fraction. The cross-sectional areas (CSAs) of cardiomyocytes and the medial thickness of the aorta in SHR + 10 (ppm) DRP and SHR + 20 (ppm) DRP groups were significantly reduced compared with SHR + NS group. The expression of ET-1 in SHR + 10DRP and SHR + 20DRP groups was significantly attenuated. These results suggest that chronic treatment with DRPs can protect against left ventricular hypertrophy and aortic remodeling. DRPs may offer a new approach to the treatment of left ventricular hypertrophy and aortic remodeling caused by hypertension.

摘要

减阻聚合物(DRPs)在微小浓度下就已被证实可以降低外周血管阻力。在这项研究中,我们评估了 DRPs 对自发性高血压大鼠(SHR)的高血压诱导的左心室肥厚和主动脉重塑的影响。雄性 SHR 和年龄匹配的 Wistar 大鼠被分为四组,分别接受生理盐水(NS)或 DRPs 的静脉注射。测量体重(BW)、心率(HR)和收缩压(SBP)。超声心动图用于评估左心室(LV)功能和整体壁运动的变化。用苏木精和伊红对 LV 和主动脉进行染色。评估每个切片的心肌细胞大小和主动脉中层厚度。通过定量逆转录聚合酶链反应(qRT-PCR)和免疫组织化学检测 LV 和主动脉内皮素-1(ET-1)的表达。在 SHR + NS、SHR + 10DRP 和 SHR + 20DRP 组中,SBP 的增加没有显著差异。SHR + NS 组的左心室收缩末期直径和左心室舒张末期直径明显较小,但前壁和后壁收缩期厚度较大,而缩短分数和射血分数没有显著差异。与 SHR + NS 组相比,SHR + 10(ppm)DRP 和 SHR + 20(ppm)DRP 组的心肌细胞横截面积(CSAs)和主动脉中层厚度明显减少。SHR + 10DRP 和 SHR + 20DRP 组的 ET-1 表达明显减弱。这些结果表明,DRPs 的慢性治疗可以预防左心室肥厚和主动脉重塑。DRPs 可能为治疗高血压引起的左心室肥厚和主动脉重塑提供一种新方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/35920b7aa274/ijn-11-6743Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/68e6b242f4a0/ijn-11-6743Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/67cc99bb6a8f/ijn-11-6743Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/09e179803f58/ijn-11-6743Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/b5fda3de9a59/ijn-11-6743Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/1665f4af3d02/ijn-11-6743Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/35920b7aa274/ijn-11-6743Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/68e6b242f4a0/ijn-11-6743Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/67cc99bb6a8f/ijn-11-6743Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/09e179803f58/ijn-11-6743Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/b5fda3de9a59/ijn-11-6743Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/1665f4af3d02/ijn-11-6743Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/5167458/35920b7aa274/ijn-11-6743Fig6.jpg

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本文引用的文献

1
Structural remodeling of the heart and its premotor cardioinhibitory vagal neurons following T(5) spinal cord transection.T(5)脊髓横断后心脏及其运动前心抑制性迷走神经元的结构重塑。
J Appl Physiol (1985). 2014 May 1;116(9):1148-55. doi: 10.1152/japplphysiol.01285.2013. Epub 2014 Mar 7.
2
New insights into the microvascular mechanisms of drag reducing polymers: effect on the cell-free layer.关于减阻聚合物的微血管机制的新见解:对无细胞层的影响。
PLoS One. 2013 Oct 4;8(10):e77252. doi: 10.1371/journal.pone.0077252. eCollection 2013.
3
Hydrostatic pressure and shear stress affect endothelin-1 and nitric oxide release by endothelial cells in bioreactors.
宽根抑制自发性高血压大鼠的动脉重塑。
Exp Ther Med. 2017 Dec;14(6):5395-5400. doi: 10.3892/etm.2017.5218. Epub 2017 Sep 28.
静水压和切应力会影响生物反应器内皮细胞内皮素-1 和一氧化氮的释放。
Biotechnol J. 2014 Jan;9(1):146-54. doi: 10.1002/biot.201300016. Epub 2013 Sep 17.
4
Reduced hemodynamic load aids low-dose resveratrol in reversing cardiovascular defects in hypertensive rats.低剂量白藜芦醇减轻血流动力学负荷可逆转高血压大鼠的心血管缺陷。
Hypertens Res. 2013 Oct;36(10):866-72. doi: 10.1038/hr.2013.55. Epub 2013 Jun 20.
5
Effect of farnesyltransferase inhibition on cardiac remodeling in spontaneously hypertensive rats.法尼基转移酶抑制剂对自发性高血压大鼠心脏重构的影响。
Int J Cardiol. 2013 Oct 9;168(4):3340-7. doi: 10.1016/j.ijcard.2013.04.038. Epub 2013 May 9.
6
A new hydrodynamic approach by infusion of drag-reducing polymers to improve left ventricular function in rats with myocardial infarction.一种新的流体动力学方法,通过输注减阻聚合物来改善心肌梗死后大鼠的左心室功能。
Int J Cardiol. 2011 Feb 17;147(1):112-7. doi: 10.1016/j.ijcard.2010.09.008. Epub 2011 Jan 5.
7
Cardiovascular changes in spontaneously hypertensive rats are improved by chronic treatment with zofenopril.自发性高血压大鼠的心血管变化可通过佐芬普利的慢性治疗得到改善。
Br J Pharmacol. 2009 Dec;158(8):1911-21. doi: 10.1111/j.1476-5381.2009.00491.x.
8
Mechanotransduction in vascular physiology and atherogenesis.血管生理学和动脉粥样硬化形成中的机械转导
Nat Rev Mol Cell Biol. 2009 Jan;10(1):53-62. doi: 10.1038/nrm2596.
9
A novel hydrodynamic approach to the treatment of coronary artery disease.一种治疗冠状动脉疾病的新型流体动力学方法。
Eur Heart J. 2006 Oct;27(19):2362-9. doi: 10.1093/eurheartj/ehl165. Epub 2006 Aug 16.
10
Elastic fibres and vascular structure in hypertension.高血压中的弹性纤维与血管结构
Pharmacol Ther. 2006 Sep;111(3):771-91. doi: 10.1016/j.pharmthera.2005.12.003. Epub 2006 Feb 20.