Xanthine oxidoreductase inhibition causes reverse remodeling in rats with dilated cardiomyopathy

Khalid M. Minhas, Roberto M. Saraiva, Karl H. Schuleri, Stephanie Lehrke, Meizi Zheng, Anastasios P. Saliaris, Cristine E. Berry, Konrad M. Vandegaer, Dechun Li, Joshua M. Hare

Research output: Contribution to journalArticlepeer-review

136 Scopus citations


Increased reactive oxygen species (ROS) generation is implicated in cardiac remodeling in heart failure (HF). As xanthine oxidoreductase (XOR) is 1 of the major sources of ROS, we tested whether XOR inhibition could improve cardiac performance and induce reverse remodeling in a model of established HF, the spontaneously hypertensive/HF (SHHF) rat. We randomized Wistar Kyoto (WKY, controls, 18 to 21 months) and SHHF (19 to 21 months) rats to oxypurinol (1 mmol/L; n=4 and n=15, respectively) or placebo (n=3 and n=10, respectively) orally for 4 weeks. At baseline, SHHF rats had decreased fractional shortening (FS) (31±3% versus 67±3% in WKY, P2+ handling pathways, supporting the idea that inhibiting XOR-derived oxidative stress substantially improves the HF phenotype.

Original languageEnglish (US)
Pages (from-to)271-279
Number of pages9
JournalCirculation Research
Issue number2
StatePublished - Feb 2006


  • Gene expression
  • Heart failure
  • Remodeling
  • Xanthine oxidoreductase

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine


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