VENTRICULAR HYPERTROPHY AND ARTERIAL HEMODYNAMICS FOLLOWING DEPRIVATION OF NITRIC OXIDE IN RATS

作者: Cheng-Tao Hu , Huai-Ren Chang , Yung-Hsiang Hsu , Chia-Jui Liu , Hsing I. Chen

DOI: 10.1016/J.LFS.2005.04.061

关键词:

摘要: Abstract In the present study, we elucidated possible role of hemodynamic parameters and chemical factors in development ventricular hypertrophy (VH) following chronic nitric oxide (NO) deprivation with N ω -nitro- l -arginine methyl ester ( l- NAME). Impedance spectral analysis was used to obtain arterial hemodynamics including steady pulsatile components. Body weight (BW), left (LV) (LVW), LVW / BW ratio, LV collagen volume fraction (LVCVF), cyclic GMP, nitrite/nitrate were measured. The extent VH evaluated by LW/BW, total number, numerical density, size cardiomyocytes. Sprague–Dawley rats given NAME 10, 20, 40 mg/kg/day from age 10 18 weeks. Control age-matched vehicle for same period. Treatment 8 weeks caused a dose-dependent increase tail cuff pressure reduction BW increases LVW, LVW/BW, myocytes. There elevation aortic decreases cardiac output, compliance. peripheral resistance, characteristic impedance pulse wave reflection increased. Histological finding revealed severe myocardial fibrosis fibroblast infiltration. LVCVF increased, while cGMP reduced manner. results suggest that NOS blockade causes hypertension, impairment large vessel properties, VH. may result partly ventricle. Correlation indicates is equally related hemodynamics.

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