Aminoguanidine Prevents Age-Related Deterioration in Left Ventricular- Arterial Coupling in Fisher 344 Rats

1 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. 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. 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. 3 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. 4 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