Retention of sarcoplasmic calcium inhibits development of the phencyclidine-restraint experimental myopathy.
The myopathy induced in the rat by the central nervous system stimulant, phencyclidine (PCP), and restraint is characterized by extensive myofibrillar sarcomere disruption in hind limb muscles and massive increases in plasma creatine kinase (CPK) activity. The effects of dantrolene sodium on this myopathy were studied to determine if modulation of calcium release from the sarcoplasmic reticulum could alter the development of the myopathy. Dantrolene prevented both the sarcomere disruption and the increase in plasma CPK activity produced in the PCP-restraint model. The inhibitory effect was not due to a decrease in the locomotor activity produced by PCP. The findings are consistent with a role for excess sarcoplasmic calcium, originating from the sarcoplasmic reticulum, in the development of this myopathy.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003402:Creatine Kinase / Q000097:blood; D008297:Male; D009132:Muscles / Q000473:pathology; D009135:Muscular Diseases / Q000097:blood / Q000139:chemically induced / Q000209:etiology* / Q000473:pathology; D010622:Phencyclidine; D051381:Rats; D011919:Rats, Inbred Strains; D012149:Restraint, Physical; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*
D003402:Creatine Kinase; D010622:Phencyclidine; D002118:Calcium