Abstract
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 language | English (US) |
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Pages (from-to) | 271-279 |
Number of pages | 9 |
Journal | Circulation Research |
Volume | 98 |
Issue number | 2 |
DOIs | |
State | Published - Feb 2006 |
Keywords
- Gene expression
- Heart failure
- Remodeling
- Xanthine oxidoreductase
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine