Key result
In dogs with heart failure, NOS inhibition prevented the +26.2% and +66.5% enhancements of contractility and efficiency observed with allopurinol, indicating NOS-XO crosstalk regulates energetics.
Why the study?
Does the balance between xanthine oxidase and nitric oxide synthase signaling regulate myocardial mechanical efficiency in normal and failing hearts?
Does the balance between xanthine oxidase and nitric oxide synthase signaling regulate myocardial mechanical efficiency in normal and failing hearts?
Upregulation of xanthine oxidase relative to nitric oxide synthase contributes to mechanoenergetic uncoupling in heart failure, and inhibition of XO improves cardiac efficiency via a NOS-dependent antioxidant mechanism.
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NOS-XO crosstalk may regulate energetics in failing hearts; leaves open whether XO inhibition benefits patients.
Saavedra et al. (2002) studied Heart failure (pacing-induced in dogs). Ascorbate, Allopurinol, and L-NMMA vs. Baseline/Normal hearts was evaluated on Myocardial mechanical efficiency and contractility. In dogs with heart failure, NOS inhibition prevented the +26.2% and +66.5% enhancements of contractility and efficiency observed with allopurinol, indicating NOS-XO crosstalk regulates energetics.
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