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Ventricular hypertrophy and arterial hemodynamics following deprivation of nitric oxide in rats

机译：大鼠一氧化氮被剥夺后心室肥大和动脉血流动力学

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摘要

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 N-omega-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 nitriteitrate 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 nitriteitrate 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 nitriteitrate in the ventricle. Correlation analysis indicates that the extent of VH is equally related to the steady and pulsatile hemodynamics. (c) 2005 Elsevier Inc. All rights reserved.
机译：在本研究中，我们阐明了在用N-ω-硝基-L-精氨酸甲酯（L-NAME）剥夺慢性一氧化氮（NO）后，血流动力学参数和化学因素在心室肥大（VH）发生中的可能作用。阻抗谱分析用于获得包括稳定和搏动成分在内的动脉血流动力学。测量体重（BW），左心室（LV）重量（LVW），LVW / BW比，LV胶原蛋白体积分数（LVCVF），循环GMP和亚硝酸盐/硝酸盐。 VH的程度通过LW / BW，总数，数值密度和心肌细胞大小进行评估。从10到18周的年龄开始，对Sprague-Dawley大鼠给予L，NAME 10、20和40 mg / kg /天。对照和年龄匹配的大鼠在同一时期给予媒介物。 L-NAME治疗8周后，随着LVW，LVW / BW，数量，数量密度和心肌细胞数量的增加，尾袖压和BW降低均呈剂量依赖性。主动脉压力升高，心输出量降低，动脉顺应性降低。总的外围电阻，特征阻抗和脉冲波反射都增加了。组织学检查发现严重的心肌肥大和纤维化伴成纤维细胞浸润。 LVCVF增加，而LV cGMP和亚硝酸盐/硝酸盐以剂量依赖的方式减少。结果表明，慢性NOS阻滞会导致高血压，大血管特性受损和VH。 VH的发展可能部分归因于心室中cGMP和亚硝酸盐/硝酸盐的减少。相关分析表明，VH的程度与稳定和搏动的血流动力学同等相关。 （c）2005 Elsevier Inc.保留所有权利。

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