Beta adrenergic-mediated myofibrillar disruption and enzyme efflux in an experimental myopathy related to isometric muscle activity

Ralph W. Kuncl*, Herbert Y. Meltzer

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Adrenal demedullation significantly inhibits the enormous increase in plasma creatine phosphokinase (CPK) activity and myofibrillar disruption which follow treatment with phencyclidine (PCP) and restraint in the rat. To determine if the effects of adrenal demedullation were due to the lack of epinephrine, we studied the effects of the β-adrenergic receptor blockers, propranolol and 3-morpholino-4-[3-t-butyl-amino-2-hydroxypropoxy]-1,2,5-thiadiazole hydrogen maleate (MK-950) on these myopathic parameters in intact rats subjected to PCP plus restraint. Both drugs significantly inhibited the myopathy. Pretreatment with either phenoxybenzamine, at effective α-adrenergic receptor blocking doses, or atropine, at effective antimuscarinic anticholinergic doses, had no effect on these parameters. Plasma CPK activity and the percentage of muscle fibers with extensive myofibrillar disruptions following PCP and restraint were significantly correlated for all treatments, except phenoxybenzamine (r = +0.71, N = 17, P < 0.001). These findings indicate the importance of adrenal epinephrine to the etiology of this myopathy. It is proposed that epinephrine stimulates a β-adrenergic process which ultimately leads to a hypoxic state and muscle injury.

Original languageEnglish (US)
Pages (from-to)113-123
Number of pages11
JournalExperimental and Molecular Pathology
Volume31
Issue number1
DOIs
StatePublished - Jan 1 1979

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Clinical Biochemistry

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