https://scholars.lib.ntu.edu.tw/handle/123456789/507175
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | YI-TSEN LIN | en_US |
dc.contributor.author | Tseng Y.-Z. | en_US |
dc.contributor.author | KUO-CHU CHANG | en_US |
dc.creator | Lin Y.-T.;Tseng Y.-Z.;Kuo-Chu Chang | - |
dc.date.accessioned | 2020-06-30T07:47:04Z | - |
dc.date.available | 2020-06-30T07:47:04Z | - |
dc.date.issued | 2004 | - |
dc.identifier.issn | 1535-3702 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-7244232533&doi=10.1177%2f153537020422901008&partnerID=40&md5=f02ce2e94c7a2054fe979f3f0a1bc36f | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/507175 | - |
dc.description.abstract | 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. | en_US |
dc.publisher | Society for Experimental Biology and Medicine | en_US |
dc.relation.ispartof | Experimental Biology and Medicine | en_US |
dc.subject | Advanced glycation end products; Aminoguanidine; Aortic input impedance; Fructose; Pulse wave reflection | en_US |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | 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 | - |
dc.title | Aminoguanidine prevents fructose-induced arterial stiffening in Wistar rats: Aortic impedance analysis | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1177/153537020422901008 | - |
dc.identifier.pmid | 15522840 | - |
dc.identifier.scopus | 2-s2.0-7244232533 | - |
dc.relation.pages | 1038-1045 | en_US |
dc.relation.journalvolume | 229 | en_US |
dc.relation.journalissue | 10 | en_US |
item.cerifentitytype | Publications | - |
item.fulltext | no fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.openairetype | journal article | - |
item.grantfulltext | none | - |
crisitem.author.dept | Otolaryngology-NTUH | - |
crisitem.author.dept | Otolaryngology | - |
crisitem.author.dept | Physiology | - |
crisitem.author.orcid | 0000-0002-4421-5711 | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
顯示於: | 生理學科所 |
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