Aminoguanidine prevents fructose-induced arterial stiffening in Wistar rats: aortic impedance analysis.

摘要: Fructose has been reported as a potent agent in forming advanced glycation end products (AGEs) and, thus, may play significant role the pathogenesis of diabetic complications. Herein, we determined effects aminoguanidine (AG), an inhibitor AGEs, on mechanical properties arterial system fructose-fed (FF) rats, using aortic impedance analysis. Rats at 2 months were given 10% fructose drinking water for weeks and compared with untreated age-matched controls. Meanwhile, FF rats treated AG (daily peritoneal injections 50 mg kg(-1)) group. Neither nor affects body weight, blood glucose level, basal heart rate. In comparison controls, showed decrease cardiac output absence any changes mean pressure, having increased total peripheral resistance (R(p)), 51.1 +/- 2.9 versus 66.2 1.9 mm Hg sec ml(-1) (P < 0.05). also contributed to increase characteristic (Z(c)), from 1.528 0.094 1.933 0.084 ml (-1) 0.05) wave transit time (tau), 22.6 0.6 19.2 0.7 msec The elevated Z(c) reduced tau suggest that cause detriment distensibility animals. After exposure AG, exhibited improvement physical vessels, evidenced by reduction 21.3% R(p). retarded fructose-induced decline distensibility, reflected 16.0% 18.1% By contrast, exerted no Windkessel well normal diet We conclude prevent fructose-derived stiffening, possibly through inhibition product formation Wistar rats.