Delayed treatment effects of xanthine oxidase inhibition on systolic overload-induced left ventricular hypertrophy and dysfunction.

Nucleosides Nucleotides Nucleic Acids

Cardiovascular Division, Department of Medicine, University of Minnesota, The Center of Vascular Biology, Minneapolis, Minnesota 55455, USA.

Published: June 2010

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 ( approximately 10% increase in LV ejection fraction). However, the purine analog allopurinol tended to increase mortality compared with vehicle or febuxostat in HF mice.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903770PMC
http://dx.doi.org/10.1080/15257771003738683DOI Listing

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