Abstract：
:In the present study, we elucidated the possible role of hemodynamic parameters and chemical factors in the development of ventricular hypertrophy (VH) following chronic nitric oxide (NO) deprivation with Nomega-nitro-L-arginine methyl ester (L-NAME). Impedance spectral analysis was used to obtain the arterial hemodynamics including the steady and pulsatile components. Body weight (BW), left ventricular (LV) weight (LVW), LVW/BW ratio, LV collagen volume fraction (LVCVF), cyclic GMP, and nitrite/nitrate were measured. The extent of VH was evaluated by the LW/BW, total number, numerical density, and size of cardiomyocytes. Sprague-Dawley rats were given L-NAME 10, 20, and 40 mg/kg/day from the age of 10 to 18 weeks. Control and age-matched rats were given vehicle for the same period. Treatment of L-NAME for 8 weeks caused a dose-dependent increase in tail cuff pressure and a reduction in BW with increases in LVW, LVW/BW, number, numerical density, and size of myocytes. There was elevation of aortic pressure with decreases in cardiac output, and arterial compliance. The total peripheral resistance, characteristic impedance and pulse wave reflection were increased. Histological finding revealed severe myocardial hypertrophy and fibrosis with fibroblast infiltration. The LVCVF was increased, while LV cGMP and nitrite/nitrate were reduced in a dose-dependent manner. The results suggest that chronic NOS blockade causes hypertension, impairment of large vessel properties, and VH. The development of VH may result partly from the decreases in cGMP and nitrite/nitrate in the ventricle. Correlation analysis indicates that the extent of VH is equally related to the steady and pulsatile hemodynamics.
journal_name
Life Scijournal_title
Life sciencesauthors
Hu CT,Chang HR,Hsu YH,Liu CJ,Chen HIdoi
10.1016/j.lfs.2005.04.061subject
Has Abstractpub_date
2005-11-26 00:00:00pages
164-73issue
2eissn
0024-3205issn
1879-0631pii
S0024-3205(05)00687-9journal_volume
78pub_type
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