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肌浆钙的潴留可抑制苯环己哌啶约束实验性肌病的发展。

Retention of sarcoplasmic calcium inhibits development of the phencyclidine-restraint experimental myopathy.

作者信息

Ross-Canada J, Chizzonite R A, Meltzer H Y

出版信息

Exp Neurol. 1983 Jan;79(1):1-10. doi: 10.1016/0014-4886(83)90373-4.

DOI:10.1016/0014-4886(83)90373-4
PMID:6822247
Abstract

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.

摘要

中枢神经系统兴奋剂苯环利定(PCP)和束缚诱导大鼠产生的肌病,其特征为后肢肌肉中广泛的肌原纤维肌节破坏以及血浆肌酸激酶(CPK)活性大幅增加。研究了丹曲林钠对这种肌病的影响,以确定肌浆网钙释放的调节是否会改变肌病的发展。丹曲林可预防PCP-束缚模型中产生的肌节破坏和血浆CPK活性增加。这种抑制作用并非由于PCP产生的运动活性降低所致。这些发现与肌浆网中过量的肌浆钙在这种肌病发展中的作用一致。

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Retention of sarcoplasmic calcium inhibits development of the phencyclidine-restraint experimental myopathy.肌浆钙的潴留可抑制苯环己哌啶约束实验性肌病的发展。
Exp Neurol. 1983 Jan;79(1):1-10. doi: 10.1016/0014-4886(83)90373-4.
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