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
收藏
页码：306 / 313
页数：8
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