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

X. Xu, L. Zhao, X. Hu, P. Zhang, J. Wessale, R. Bache, Y. Chen

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)306-313
Number of pages8
JournalNucleosides, Nucleotides and Nucleic Acids
Volume29
Issue number4-6
DOIs
StatePublished - Jun 2010

Bibliographical note

Funding Information:
This study was sponsored by Takeda Global Research & Development Center, Inc., Deerfield IL, USA. The authors are grateful to Karen Asin, Ph.D. (Takeda) for her critical and thorough reviews of the manuscript during its preparation. J. W. was a contractor for TAP Pharmaceutical Products, Inc. (now Takeda Global Research & Development Center, Inc.) during this study and is now an independent consultant. Address correspondence to Yingjie Chen, University of Minnesota, Mayo Mail Code 508, 420 Delaware St. SE, Minneapolis, MN 55455. E-mail: chenx106@tc.umn.edu

Keywords

  • Febuxostat
  • allopurinol
  • heart failure
  • left ventricular dysfunction

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