title: Aminoguanidine prevents fructose-induced deterioration in left ventricular-arterial coupling in Wistar rats.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  Rats given 10% fructose in drinking water (FF) were daily treated with AG (50 mg x 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.
  
  
  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 E(es) and Q(load) exhibited a decline with fructose feeding but showed a significant rise after AG treatment in the FF rats.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan. kcchang@hs.mc.ntu.edu.tw
authors.forename: K-C
authors.initials: KC
authors.lastname: Chang
authors.forename: J-T
authors.initials: JT
authors.lastname: Liang
authors.forename: C-D
authors.initials: CD
authors.lastname: Tseng
authors.forename: E-T
authors.initials: ET
authors.lastname: Wu
authors.forename: K-L
authors.initials: KL
authors.lastname: Hsu
authors.forename: M-S
authors.initials: MS
authors.lastname: Wu
authors.forename: Y-T
authors.initials: YT
authors.lastname: Lin
authors.forename: Y-Z
authors.initials: YZ
authors.lastname: Tseng
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D002302:Cardiac Output / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005632:Fructose / Q000008:administration & dosage / Q000633:toxicity*; D006146:Guanidines / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D051381:Rats; D017208:Rats, Wistar; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*
chemical_list: D004791:Enzyme Inhibitors; D006146:Guanidines; D005632:Fructose; D019001:Nitric Oxide Synthase; C004479:pimagedine