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Somatosens Mot Res ; 38(1): 90-94, 2021 03.
Article in English | MEDLINE | ID: mdl-33263458

ABSTRACT

INTRODUCTION: Drug-induced myopathy is among the most common causes of muscle disease. Lipid-lowering drugs, primarily the statins as inhibitors of the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, are a common cause of myopathy. Statin-fibrate combination potentially increases risk for myopathy and rhabdomyolysis. Blood levels of the enzymes creatine kinase (CK), aldolase and lactate dehydrogenase (LDH) increase during myopathy. Exercise may be a trigger for statin-associated muscle symptoms (SAMS). METHODS: In this study a model of myopathy induction was designed via combination of oral atorvastatin, gemfibrozil and exercise for ten days in rats. To maximise exercise, the rats were placed in a pool of water and allowed to swim before sinking in the last three days. Finally, the mean of swimming tolerance times and blood levels of creatine kinase, aldolase and lactate dehydrogenase were measured. RESULTS: The results showed a significantly (p < 0.05) decreased swimming tolerance time and elevated enzyme levels in rats receiving atorvastatin (ATV) and gemfibrozil (GMF) plus exercise compared with those rats in other groups. This animal model can be used to evaluate the effects of medication on reduction of statin/fibrate-induced myopathy.


Subject(s)
Hydroxymethylglutaryl-CoA Reductase Inhibitors , Muscular Diseases , Animals , Atorvastatin/toxicity , Disease Models, Animal , Fibric Acids , Gemfibrozil/toxicity , Hydroxymethylglutaryl-CoA Reductase Inhibitors/toxicity , Muscular Diseases/chemically induced , Rats
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