title: A novel hydrodynamic approach of drag-reducing polymers to improve left ventricular hypertrophy and aortic remodeling in spontaneously hypertensive rats.
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.
authors.affiliation: Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou.
authors.forename: Xinlu
authors.initials: X
authors.lastname: Zhang
authors.affiliation: 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.
authors.forename: Xu
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou.
authors.forename: Feng
authors.initials: F
authors.lastname: Hu
authors.affiliation: Department of Cardiology, Key Laboratory of Molecular Cardiovascular Sciences of Ministry of Education, and Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides of Ministry of Health, Peking University Third Hospital, Beijing.
authors.forename: Boda
authors.initials: B
authors.lastname: Zhou
authors.affiliation: Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou.
authors.forename: Hai-Bin
authors.initials: HB
authors.lastname: Chen
authors.affiliation: Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou.
authors.forename: Daogang
authors.initials: D
authors.lastname: Zha
authors.affiliation: Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou.
authors.forename: Yili
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Department of Cardiovascular Medicine, Fujian Provincial Hospital, Fuzhou, People's Republic of China.
authors.forename: Yansong
authors.initials: Y
authors.lastname: Guo
authors.affiliation: 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.
authors.forename: Lemin
authors.initials: L
authors.lastname: Zheng
authors.affiliation: Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou.
authors.forename: Jiancheng
authors.initials: J
authors.lastname: Xiu
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000473:pathology; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002317:Cardiovascular Agents / Q000008:administration & dosage / Q000494:pharmacology*; D004562:Electrocardiography; D019332:Endothelin-1 / Q000235:genetics / Q000378:metabolism; D006339:Heart Rate / Q000187:drug effects; D006973:Hypertension / Q000150:complications / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D007262:Infusions, Intravenous; D008297:Male; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000473:pathology; D011108:Polymers / Q000008:administration & dosage / Q000494:pharmacology*; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D066253:Vascular Remodeling
chemical_list: D002317:Cardiovascular Agents; D019332:Endothelin-1; D011108:Polymers
keywords: ET-1; aortic remodeling; drag-reducing polymers; hypertension; left ventricular hypertrophy