Aminoguanidine prevents age-related aortic stiffening in Fisher 344 rats: aortic impedance analysis

被引:10
作者
Chang, KC
Hsu, KL
Peng, YI
Lee, FC
Tseng, YZ
机构
[1] Natl Taiwan Univ, Coll Med, Dept Physiol, Taipei, Taiwan
[2] Natl Taiwan Univ Hosp, Taipei, Taiwan
关键词
advanced glycation end products; AG; aortic input impedance; aortic distensibility; pulsatile wave reflection;
D O I
10.1038/sj.bjp.0705410
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
1 We determined the effects of long-term treatment with aminoguanidine (AG), an inhibitor of advanced glycation end products, on the mechanical properties of the arterial system in aged Fisher 344 rats, using the aortic impedance analysis. 2 Normotensive rats were treated from 18 to 24 months with AG (1 g/l(-1) in drinking water) and compared with a control group. Pulsatile aortic pressure and flow signals were measured and then subjected to Fourier transformation for the analysis of aortic input impedance. Wave transit time was determined using the impulse response function of the filtered aortic input impedance spectra. 3 With no alteration in body weight, rats treated with AG had decreased heart weight compared with the aged untreated controls. 4 AG did not affect arterial blood pressure; however, the age-related increase in total peripheral resistance was prevented by AG. 5 AG retarded the age-related decline in aortic distensibility, as evidenced by a reduction of 25.2% in aortic characteristic impedance and an increase of 28.1% in wave transit time. 6 Meanwhile, the increase in wave reflection factor in aging rats was reduced by 32.3% by AG. Both the increased wave transit time and the decreased wave reflection factor suggest that AG may prevent the aee-related augmentation in systolic loading condition for the left ventricle coupled to the arterial system. 7 We conclude that long-term treatment with AG may impart significant protection against aortic stiffening and cardiac hypertrophy in aged Fisher 344 rats.
引用
收藏
页码:107 / 114
页数:8
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