A novel hydrodynamic approach of drag-reducing polymers to improve left ventricular hypertrophy and aortic remodeling in spontaneously hypertensive rats.
A novel hydrodynamic approach of drag-reducing polymers to improve left ventricular hypertrophy and aortic remodeling in spontaneously hypertensive rats.
复制标题
一种新的减阻聚合物流体动力学方法，可改善自发性高血压大鼠的左心室肥厚和主动脉重塑。
DOI：
10.2147/ijn.s119607
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发表时间：
2016
影响因子：
8
通讯作者：
Xiu J
中科院分区：
文献类型：
--
作者：
Zhang X;Wang X;Hu F;Zhou B;Chen HB;Zha D;Liu Y;Guo Y;Zheng L;Xiu J
减阻聚合物（DRPs）在微量添加时，已被证明可降低外周血管阻力。在本研究中，对自发性高血压大鼠（SHR）评估了DRPs对高血压诱导的左心室肥厚和主动脉重塑的影响。将雄性SHR和年龄匹配的Wistar大鼠分为四组，并接受生理盐水（NS）或DRPs的静脉注射。测量体重（BW）、心率（HR）和收缩压（SBP）。使用超声心动图评估左心室（LV）功能和整体室壁运动的变化。用苏木精和伊红对左心室和主动脉进行染色。对每个切片评估心肌细胞的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左心室和主动脉内皮素 - 1（ET - 1）的表达。在SHR + NS、SHR + 10DRP和SHR + 20DRP组之间，收缩压的升高没有显著差异。SHR + NS组的左心室收缩末期内径和左心室舒张末期内径明显较小，但前、后收缩期室壁厚度较大，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组和SHR + 20（ppm）DRP组的心肌细胞横截面积（CSAs）和主动脉中层厚度显著降低。SHR + 10DRP组和SHR + 20DRP组中ET - 1的表达显著减弱。这些结果表明，DRPs长期治疗可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。
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.