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

• Published in: British journal of pharmacology Vol. 151; no. 3; pp. 341 - 346
• Main Authors: Chang, K‐C, Liang, J‐T, Tseng, C‐D, Wu, E‐T, Hsu, K‐L, Wu, M‐S, Lin, Y‐T, Tseng, Y‐Z
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.06.2007; Nature Publishing; Nature Publishing Group
• Subjects: aminoguanidine; Analysis of Variance; Animals; Biological and medical sciences; Blood Pressure - drug effects; Cardiac Output - drug effects; effective arterial volume elastance; end‐systolic elastance; Enzyme Inhibitors - pharmacology; Fructose - administration & dosage; Fructose - toxicity; fructose loading; Guanidines - pharmacology; Heart Rate - drug effects; Male; Medical sciences; Nitric Oxide Synthase - antagonists & inhibitors; Pharmacology. Drug treatments; Rats; Rats, Wistar; Research Papers; Ventricular Dysfunction, Left - etiology; Ventricular Dysfunction, Left - physiopathology; Ventricular Dysfunction, Left - prevention & control; ventricular–arterial coupling; effective arterial volume elastance; Vertebrata; Aminoguanidine; Mammalia; Rat; Animal; Rodentia; ventricular-arterial coupling; end-systolic elastance; fructose loading; Fructose
• ISSN: 0007-1188; 1476-5381
• DOI: 10.1038/sj.bjp.0707223

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 (50 mg·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 (Ees, an indicator of myocardial contractility) and effective arterial volume elastance (Ea). The optimal afterload (Qload) determined by the ratio of Ea to Ees 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 Ea. Fructose loading significantly elevated Ea and AG prevented the fructose‐derived deterioration in arterial chamber elastance. Both fructose and AG affected Ees and Qload, 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) 151, 341–346; doi:10.1038/sj.bjp.0707223