SUCCINYLCHOLINE-INDUCED FASCICULATIONS IN DENERVATED RAT MUSCLES AS MEASURED USING P-31-NMR SPECTROSCOPY - THE EFFECT OF PRETREATMENT WITH DANTROLENE OR VECURONIUM
M. Mizogami et al., SUCCINYLCHOLINE-INDUCED FASCICULATIONS IN DENERVATED RAT MUSCLES AS MEASURED USING P-31-NMR SPECTROSCOPY - THE EFFECT OF PRETREATMENT WITH DANTROLENE OR VECURONIUM, Acta anaesthesiologica Scandinavica, 42(4), 1998, pp. 472-477
Background: We have previously demonstrated by P-31 nuclear magnetic r
esonance (NMR) that succinylcholine (SCh) induces metabolic changes in
denervated muscle. To specify those changes, we attempted to inhibit
them using two different kinds of drugs, dantrolene and vecuronium. Me
thods: Three weeks after unilateral sciatic nerve section, 75 male Wis
tar rats were randomly assigned to one of the following 5 groups: (1)
non-pretreated normal muscle group; (2) non-pretreated denervated musc
le group; (3) denervated muscle group pretreated with a low dose of ve
curonium (0.02 mg.kg(-1)); (4) denervated muscle group pretreated with
a high dose of vecuronium (0.2 mg.kg(-1)); (5) denervated muscle grou
p pretreated with dantrolene (2 mg.kg(-1)). The change of the inorgani
c phosphate/phosphocreatine (Pi/PCr) ratio of each muscle was measured
by P-31-NMR before and after SCh (1 mg.kg(-1)) administration and the
corresponding peak amplitude of the electromyograms (EMG) was determi
ned. Results: The high dose of vecuronium totally inhibited SCh-induce
d fasciculation on EMG (100%-->2%). In this group, though the Pi/PCr r
atio significantly increased 10 min after SCh, the peak after 5 min di
sappeared. The inhibition with dantrolene was about the same order of
magnitude as with the low dose of vecuronium (35%:21%). However, the i
ncrease in the Pi/PCr only lasted about 10 min, in contrast to the oth
er drugs. Conclusion: Our findings indicate that the Pi/PCr increases
5 and 10 min after SCh, respectively, as a result of two different pro
cesses. The first peak is caused by an excessive energy consumption in
response to excessive muscle contraction. This in turn triggers the s
econd peak, caused by breakdown of glycogen, initiated by an increased
Ca2+ concentration.