Aminoguanidine prevents fructose-induced deterioration in left ventricular-arterial coupling in Wistar rats

Background and purpose: Aminoguanidine (AG), an inhibitor of advanced glycation endproducts, has been identified as a prominent agent that prevents the fructose-induced arterial stiffening in male Wistar rats. Our aims were to examine whether AG produced benefits on the left ventricular ( LV)-arterial coupling in fructose-fed ( FF) animals in terms of the ventricular and arterial chamber properties. Experimental approach: Rats given 10% fructose in drinking water ( FF) were daily treated with AG ( 50mg . kg(-1), i. p.) for 2 weeks and compared with the untreated FF group. In anaesthetised rats, LV pressure and ascending aortic flow signals were recorded to calculate LV end-systolic elastance ( E-es, an indicator of myocardial contractility) and effective arterial volume elastance ( E-a). The optimal afterload ( Q(load)) determined by the ratio of E-a to E-es was used to measure the coupling efficiency between the left ventricle and its vasculature. Key results: There was a significant interaction between fructose and AG in their effects on E-a. Fructose loading significantly elevated E-a and AG prevented the fructose- derived deterioration in arterial chamber elastance. Both fructose and AG affected E-es and Q(load), and there was an interaction between fructose and AG for these two variables. Both Ees and Qload exhibited a decline with fructose feeding but showed a significant rise after AG treatment in the FF rats. Conclusions and Implications: AG prevented not only the contractile dysfunction of the heart caused by fructose loading, but also the fructose- induced deterioration in matching left ventricular function to the arterial system. British Journal of Pharmacology ( 2007).