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Creatine kinase and prostaglandin E, release from isolated Duchenne muscle

Department of Medicine (Drs. Jackson and Edwards), University of Liverpool, Liverpool, UK; and the Jerry Lewis Muscle Research Center, Department of Neurology (Drs. Brooke and Kaiser), Washington University School of Medicine, St. Louis, MO.

We studied the release of creatine kinase (CK) activity and prostaglandin E₂ (PGE₂ from isolated strips of biceps muscle from patients with Duchenne muscular dystrophy and nondystrophic control patients. CK release was significantly higher from the dystrophic samples than controls during the initial period of incubation, but this difference reduced with time of incubation. Immediate immersal of muscle strips into calcium-free bathing medium reduced the initial difference between the efflux from dystrophic and nondystrophic samples, whereas treatment with the calcium ionophore maintained the difference between the groups throughout the period of incubation (150 minutes). These results support the hypothesis that the lack of dystrophin in Duchenne muscle leads to damage to the tissue via a failure of calcium homeostasis. PGE₂ release from the muscle strips followed a similar pattern to CK activity, supporting the possibility that, at least partly, the calcium-mediated damage involves activation of phospholipid hydrolysis.

Address correspondence and reprint requests to Dr. M.J. Jackson, Department of Medicine, University of Liverpool, P.O. Box 147, Liverpool L69 3BX. UK.

Received January 23, 1990. Accepted for publication in final form June 27,1990.

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