Delayed Treatment Effects of Xanthine Oxidase Inhibition on Systolic Overload-Induced Left Ventricular Hypertrophy and Dysfunction

被引：14

作者：

Xu, X. ^{[1
,2
]}

Zhao, L. ^{[3
]}

Hu, X. ^{[1
,2
]}

Zhang, P. ^{[1
,2
]}

Wessale, J. ^{[3
]}

Bache, R. ^{[1
,2
]}

Chen, Y. ^{[1
,2
]}

机构：

[1] Univ Minnesota, Ctr Vasc Biol, Minneapolis, MN 55455 USA

[2] Univ Minnesota, Dept Med, Div Cardiovasc, Minneapolis, MN 55455 USA

[3] Takeda Global Res & Dev Ctr Inc, Deerfield, IL USA

来源：

NUCLEOSIDES NUCLEOTIDES & NUCLEIC ACIDS | 2010年 / 29卷 / 4-6期

关键词：

Febuxostat; allopurinol; heart failure; left ventricular dysfunction; INDUCED HEART-FAILURE; MYOCARDIAL-INFARCTION; CARDIOMYOPATHY; FEBUXOSTAT; EFFICIENCY; DOGS;

D O I：

10.1080/15257771003738683

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The nonpurine selective xanthine oxidase (XO) inhibitor febuxostat attenuates development of left ventricular (LV) hypertrophy and dysfunction in mice when treatment is initiated within 1 hour of transverse aortic constriction (TAC). This study investigated whether a 7-day delay of treatment with the XO inhibitors febuxostat or allopurinol would reverse TAC-induced changes after onset of heart failure (HF). Neither treatment significantly affected TAC-induced LV hypertrophy; only febuxostat caused a modest improvement in LV function (10% increase in LV ejection fraction). However, the purine analog allopurinol tended to increase mortality compared with vehicle or febuxostat in HF mice.

引用

页码：306 / 313

页数：8

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