https://scholars.lib.ntu.edu.tw/handle/123456789/507175
標題: | Aminoguanidine prevents fructose-induced arterial stiffening in Wistar rats: Aortic impedance analysis | 作者: | YI-TSEN LIN Tseng Y.-Z. KUO-CHU CHANG |
關鍵字: | Advanced glycation end products; Aminoguanidine; Aortic input impedance; Fructose; Pulse wave reflection | 公開日期: | 2004 | 出版社: | Society for Experimental Biology and Medicine | 卷: | 229 | 期: | 10 | 起(迄)頁: | 1038-1045 | 來源出版物: | Experimental Biology and Medicine | 摘要: | Fructose has been reported as a potent agent in forming advanced glycation end products (AGEs) and, thus, may play a significant role in the pathogenesis of diabetic complications. Herein, we determined the effects of aminoguanidine (AG), an inhibitor of AGEs, on the mechanical properties of the arterial system in fructose-fed (FF) rats, using aortic impedance analysis. Rats at 2 months were given 10% fructose in drinking water for 2 weeks and compared with untreated age-matched controls. Meanwhile, FF rats were treated for 2 weeks with AG (daily peritoneal injections of 50 mg kg-1) and compared with the untreated FF group. Neither fructose nor AG affects body weight, blood glucose level, and basal heart rate. In comparison with controls, FF rats showed a decrease in cardiac output in the absence of any significant changes in mean aortic pressure, having increased total peripheral resistance (Rp), at 51.1 ± 2.9 versus 66.2 ± 1.9 mm Hg sec ml-1 (P < 0.05). Fructose also contributed to an increase in aortic characteristic impedance (Zc), from 1.528 ± 0.094 to 1.933 ± 0.084 mm Hg sec ml-1 (P < 0.05) and a decrease in wave transit time (τ), from 22.6 ± 0.6 to 19.2 ± 0.7 msec (P < 0.05). The elevated Zc and the reduced τ suggest that fructose may cause a detriment to the aortic distensibility in animals. After exposure to AG, FF rats exhibited a significant improvement in physical properties of the resistance vessels, as evidenced by the reduction of 21.3% in Rp. Meanwhile, AG retarded the fructose-induced decline in aortic distensibility, as reflected in the decrease of 16.0% in Zc (P < 0.05) and the increase of 18.1% in τ (P < 0.05). By contrast, AG exerted no effects on the mechanical properties of Windkessel vessels, as well as resistance vessels, in normal diet controls. We conclude that AG may prevent the fructose-derived changes in arterial stiffening, possibly through inhibition of the fructose-derived advanced glycation end product formation in Wistar rats. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-7244232533&doi=10.1177%2f153537020422901008&partnerID=40&md5=f02ce2e94c7a2054fe979f3f0a1bc36f https://scholars.lib.ntu.edu.tw/handle/123456789/507175 |
ISSN: | 1535-3702 | DOI: | 10.1177/153537020422901008 | SDG/關鍵字: | advanced glycation end product; aminoguanidine; drinking water; fructose; glucose; animal experiment; aorta; artery dilatation; article; body weight; controlled study; drug exposure; feeding; glucose blood level; heart output; heart rate; impedance; male; mean arterial pressure; nonhuman; rat; rigidity; spectral sensitivity; vascular resistance; Animalia; Rattus norvegicus |
顯示於: | 生理學科所 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。