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Aminoguanidine prevents age‐related deterioration in left ventricular–arterial coupling in Fisher 344 rats
Author(s) -
Chang KuoChu,
Hsu KwanLih,
Chou TsaiFwu,
Lo HueyMing,
Tseng YungZu
Publication year - 2004
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0705831
Subject(s) - afterload , ventricle , cardiology , medicine , stroke volume , left ventricular hypertrophy , blood pressure , preload , heart rate , hemodynamics
In recent studies, aminoguanidine (AG), an inhibitor of advanced glycation endproducts, has been identified as a prominent agent that can prevent the age‐related aortic stiffening and cardiac hypertrophy. The aim of this study was to determine whether AG had effects on the left ventricular (LV)–arterial coupling in aged Fisher 344 rats in terms of the ventricular and arterial chamber properties. Normotensive rats were treated from 18 to 24 months with AG (1 g l −1 in drinking water) and compared with a control group. LV pressure and ascending aortic flow signals were recorded to construct the ventricular and arterial end‐systolic pressure–stroke volume relationships to calculate LV end‐systolic elastance ( E es ) and effective arterial volume elastance ( E a ), respectively. The optimal afterload ( Q load ) determined by the ratio of E a to E es was used to measure the efficiency of mechanical energy transferred from the left ventricle to the arterial system. In comparison with the 6‐month‐old rats, the 24‐month‐old animals had decreased E es , at 567.4±26.7 vs 639.0±20.7 mmHg ml −1 , decreased E a , at 411.5±18.6 vs 577.9±15.7 mmHg ml −1 , and decreased Q load , at 0.9428±0.0024 vs 0.9962±0.0014. Treatment with AG for 6 months did not significantly affect E es ; however, when normalized to LV weight (i.e., E esn = E es /LV weight), E esn showed a significant rise of 22.8%, suggesting that AG may retard the aging process on the intrinsic contractility of the left ventricle. On the other hand, the decrease in E a in aging rats was prevented by AG, as reflected in the increase of 19.7% in this variable ( P <0.05). The 24‐month‐old treated rats also exhibited a significant rise of 21.6% in E a / E es , causing an increase of 5.2% in Q load ( P <0.05). We conclude that in healthy older Fisher 344 rats without diabetes, long‐term treatment with AG may improve both the arterial and ventricular function and optimize the matching condition for the left ventricular–arterial coupling.British Journal of Pharmacology (2004) 142 , 1099–1104. doi: 10.1038/sj.bjp.0705831