https://scholars.lib.ntu.edu.tw/handle/123456789/507169
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | MING-SHIANG WU | en_US |
dc.contributor.author | JIN-TUNG LIANG | en_US |
dc.contributor.author | Lin Y.-D. | en_US |
dc.contributor.author | EN-TING WU | en_US |
dc.contributor.author | Tseng Y.-Z. | en_US |
dc.contributor.author | KUO-CHU CHANG | en_US |
dc.creator | Wu M.-S.;Liang J.-T.;Lin Y.-D.;Wu E.-T.;Tseng Y.-Z.;Kuo-Chu Chang | - |
dc.date.accessioned | 2020-06-30T07:47:02Z | - |
dc.date.available | 2020-06-30T07:47:02Z | - |
dc.date.issued | 2008 | - |
dc.identifier.issn | 0007-1188 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-44949237880&doi=10.1038%2fbjp.2008.119&partnerID=40&md5=1a784426cba38e555a9e9a96de71e379 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/507169 | - |
dc.description.abstract | Background and purpose: Aminoguanidine (AG), an inhibitor of advanced glycation endproducts, has been shown to prevent arterial stiffening and cardiac hypertrophy in streptozotocin (STZ) and nicotinamide (NA)-induced type 2 diabetes in rats. Our aims were to examine whether AG produced benefits on cardiac pumping mechanics in the STZ and NA-treated animals in terms of maximal systolic elastance (E max) and theoretical maximum flow (Q max). Experimental approach: After induction of type 2 diabetes, rats received daily injections of AG (50 mg kg -1, i.p.) for 8 weeks and were compared with age-matched, untreated, diabetic controls. Left ventricular (LV) pressure and ascending aortic flow signals were recorded to calculate E max and Q max, using the elastance-resistance model. Physically, E max reflects the contractility of the myocardium as an intact heart, whereas Q max has an inverse relationship with the LV internal resistance. Key results: Both type 2 diabetes and AG affected E max and Q max, and there was an interaction between diabetes and AG for these two variables. The E max and Q max were reduced in rats with type 2 diabetes, but showed a significant rise after administration of AG to these diabetic rats. Moreover, the increase in Q max corresponded to a decrease in total peripheral resistance of the systemic circulation when the STZ and NA-induced diabetic rats were treated with AG. Conclusions and implications: AG therapy prevented not only the contractile dysfunction of the heart, but also the augmentation in LV internal resistance in rats with STZ and NA-induced type 2 diabetes. ? 2008 Nature Publishing Group All rights reserved. | - |
dc.relation.ispartof | British Journal of Pharmacology | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | advanced glycation end product; aminoguanidine; nicotinamide; streptozocin; animal experiment; animal model; aorta flow; arterial stiffness; artery compliance; article; controlled study; drug effect; heart afterload; heart left ventricle pressure; heart ventricle hypertrophy; male; non insulin dependent diabetes mellitus; nonhuman; oxidative stress; priority journal; rat; statistical analysis; streptozocin diabetes; systemic vascular resistance; Animals; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Disease Models, Animal; Enzyme Inhibitors; Glycosylation End Products, Advanced; Guanidines; Heart Function Tests; Male; Myocardial Contraction; Niacinamide; Rats; Rats, Wistar; Streptozocin; Ventricular Function, Left | - |
dc.title | Aminoguanidine prevents the impairment of cardiac pumping mechanics in rats with streptozotocin and nicotinamide-induced type 2 diabetes | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1038/bjp.2008.119 | - |
dc.identifier.pmid | 18376420 | - |
dc.identifier.scopus | 2-s2.0-44949237880 | - |
dc.relation.pages | 758-764 | - |
dc.relation.journalvolume | 154 | - |
dc.relation.journalissue | 4 | - |
item.openairetype | journal article | - |
item.fulltext | no fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | Internal Medicine | - |
crisitem.author.dept | Internal Medicine-NTUH | - |
crisitem.author.dept | Surgery | - |
crisitem.author.dept | Surgery-NTUH | - |
crisitem.author.dept | Pediatrics-NTUH | - |
crisitem.author.dept | Pediatrics | - |
crisitem.author.dept | Physiology | - |
crisitem.author.orcid | 0000-0002-1940-6428 | - |
crisitem.author.orcid | 0000-0002-0264-7735 | - |
crisitem.author.orcid | 0000-0002-1463-8721 | - |
crisitem.author.orcid | 0000-0002-4421-5711 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
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