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The effect of succinylcholine on energy metabolism studied by 31 P‐NMR spectroscopy in rat denervated skeletal muscle
Author(s) -
Mizogami M.,
Fujibayashi T.,
Harada J.,
Goto Y.
Publication year - 1996
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1996.tb04465.x
Subject(s) - phosphocreatine , medicine , endocrinology , midazolam , skeletal muscle , magnesium , metabolism , energy metabolism , anesthesia , chemistry , organic chemistry , sedation
Background : The goals of this study were: (1) to demonstrate the differences of metabolic changes induced by succinylcholine (SCh) administration between normal and denervated muscle by 31 P‐NMR spectroscopy: (2) to determine whether three kinds of drugs (vecuronium, midazolam and magnesium sulfate) could prevent these metabolic changes. Methods : Following unilateral sciatic nerve section, 20 male Wistar rats were studied at three‐week intervals. After SCh 1 mg·kg ‐1 was administered intravenously, the changes of the inorganic phosphate/phosphocreatine (Pi/PCr) ratio, the β ATP/(PCr+Pi) ratio, and intracellular pH were measured by 31 P‐NMR both in normal and denervated hind limb muscles of 5 rats. The other 15 rats were allocated to the pretreatment groups by the following drugs: vecuronium 0.02 mg·kg ‐1 , midazolam 0.1 mg·kg ‐1 and magnesium sulfate 60 mg·kg ‐1 . After pretreatment 3 min before SCh administration, we measured the same parameters by 31 P‐NMR. Results: SCh administration did not change the Pi/PCr ratio in normal muscle, but significantly increased that in denervated muscle (P<0.05). This increase of the Pi/PCr ratio was also observed in all pretreated groups but was minimal as compared with that in non‐pretreatment denervated muscle. Conclusion : These data suggested that SCh administration decreased the level of “energy reserve” in denervated muscle, and that this metabolic change was not totally inhibited by vecuronium, midazolam, or magnesium sulfate.