Calcium-induced damage of skeletal muscle fibers is markedly reduced by calcium channel blockers.
Vascular perfusion of rat hind limbs with a Ca2+-free physiological solution containing ethylenediaminetetraacetate, when followed by a physiological solution with normal concentration of Ca2+, caused a marked rise of creatine kinase (CK) in the venous effluent. When calcium channel blockers were present in the perfusing solutions, no rise of CK occurred. On histological sampling of perfused muscles, CK rise was roughly correlated with muscle fiber damage of the appropriate muscles. Removal of calcium from the plasmalemma of muscle fibers appears to prevent closure of calcium channels, making the muscle fibers susceptible to a deleterious influx of extracellular calcium. This influx can be prevented by the presence of calcium channel blockers in the perfusates.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D003402:Creatine Kinase / Q000097:blood; D004110:Diltiazem / Q000627:therapeutic use; D004492:Edetic Acid; D005110:Extracellular Space / Q000378:metabolism; D008297:Male; D009132:Muscles / Q000378:metabolism; D009135:Muscular Diseases / Q000517:prevention & control*; D009543:Nifedipine / Q000627:therapeutic use; D051381:Rats; D011919:Rats, Inbred Strains; D014700:Verapamil / Q000627:therapeutic use
D002121:Calcium Channel Blockers; D004492:Edetic Acid; D014700:Verapamil; D003402:Creatine Kinase; D004110:Diltiazem; D009543:Nifedipine; D002118:Calcium