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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Atorvastatin, Atrophy, Citrate (si)-Synthase, Creatine Kinase, Heptanoic Acids, Hydroxymethylglutaryl-CoA Reductase Inhibitors, L-Lactate Dehydrogenase, Male, Mice, Mice, Inbred C57BL, Muscle, Skeletal, Myosin Heavy Chains, Nitric Oxide, Nitric Oxide Donors, Pyrroles.
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Does nitric oxide prevent atorvastatin-induced skeletal muscle dysfunction and alterations in mice? Context: Myopathy is the most common side effect of statins. Because nitric oxide (NO) has a key role in regulating skeletal muscle function, we studied whether the NO-donating atorvastatin NCX 6560 could show a better profile on skeletal muscle function and structure compared with atorvastatin. C57BL/6 mice received atorvastatin 40 mg/kg/day or an equivalent dose of NCX 6560 for 2 months. Muscle function assessed by treadmill test, serum creatine kinase (CK) activity, citrate synthase (CS) activity, and muscle histology were evaluated. Atorvastatin significantly (P < 0.001) reduced muscle endurance, increased serum CK by 6-fold, and induced muscle fiber atrophy. Conversely, NCX 6560 preserved muscle function, prevented CK increase and did not modify muscle structure. Interestingly, atorvastatin reduced CS activity, a marker for mitochondrial function, in gastrocnemius, diaphragm, and heart, whereas NCX 6560 prevented such decrease.
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These findings suggest that NO may prevent statin-induced myopathy. Final Decision: yes