Artículos de revistas
DILTIAZEM AND VERAPAMIL PROTECT DYSTROPHIN-DEFICIENT MUSCLE FIBERS OF MDX MICE FROM DEGENERATION: A POTENTIAL ROLE IN CALCIUM BUFFERING AND SARCOLEMMAL STABILITY
Muscle & Nerve. John Wiley & Sons Inc, v. 39, n. 2, n. 167, n. 176, 2009.
The lack of dystrophin in mdx mice and in Duchenne muscular dystrophy causes sarcolemmal breakdown and increased calcium influx followed by myonecrosis. We examined whether the calcium channel blockers diltiazem and verapamil protect dystrophic muscles from degeneration. Mdx mice received daily intraperitoneal injections of diltiazem or verapamil for 18 days, followed by removal of the sternomastoid, diaphragm, fibialis anterior, and cardiac muscles. Control mdx mice were injected with saline. Both drugs significantly decreased blood creatine kinase levels. Total calcium content was significantly higher in mdx muscles than in control C57BI/10. Verapamil and diltiazem reduced total calcium content only in diaphragm and cardiac muscle. Histological analysis showed that diltiazem significantly attenuated myonecrosis in diaphragm. Immunoblots showed a significant increase of calsequestrin and P-dystroglycan levels in some diltiazem- and verapamil-treated muscles. Possible interactions of these drugs with the sarcoplasmic reticulum and sarcolemma may also contribute to the improvement of the dystrophic phenotype.392167176