MUSCLE PARALYSIS BY ROCURONIUM BROMIDE DURING HALOTHANE, ENFLURANE, ISOFLURANE AND TOTAL INTRAVENOUS ANESTHESIA (REPRINTED FROM ANESTH-ANALG, VOL 77, PG 570, 1993)
H. Vanaken et al., MUSCLE PARALYSIS BY ROCURONIUM BROMIDE DURING HALOTHANE, ENFLURANE, ISOFLURANE AND TOTAL INTRAVENOUS ANESTHESIA (REPRINTED FROM ANESTH-ANALG, VOL 77, PG 570, 1993), European journal of anaesthesiology, 1994, pp. 101-102
Eighty patients were equally randomized to four different groups (n=20
) receiving 0.5-1% halothane, 1.5-2% enflurane, 1.2-1.8% isoflurane en
d-tidal concentration in 34%/66% O2/N2O, or 6.0 mg kg-1 h-1 propofol w
ithout N2O for anaesthesia and alfentanil for analgesia. Strength of t
humb adduction in response to single and train-of-four stimulation of
the ulnar nerve was quantitated. Rocuronium 0.15, 0.2, 0.25, and 0.3 m
g kg-1 were given intravenously. When maximal depression of twitch ten
sion occurred, supplementary doses up to a total of 0.5 mg kg-1 were g
iven. If required, additional doses of 0.15 mg kg-1 were given at 25%
recovery of control twitch tension. Standard haemodynamics, end-tidal
CO2, and anaesthetic gas concentrations were monitored continuously. T
he mean ED50 (SD) was 0.133 (+/-0.009) mg kg-1 for the halothane group
, 0.118 (+/-0.012) mg kg-1 for the enflurane group, 0.069 (+/-0.026) m
g kg-1 for the isoflurane group, and 0.167 (+/-0.007) mg kg-1 for the
total intravenous anaesthesia (TIVA) group, respectively. There was a
statistically significant difference between the halothane and TIVA, a
nd between the enflurane and TIVA groups (P<0.05). The neuromuscular b
locking potency and pharmacodynamic profile of rocuronium are moderate
ly influenced by volatile anaesthetics.