Neuromuscular and cardiovascular effects of mivacurium chloride in surgical patients receiving nitrous oxide-narcotic or nitrous oxide-isoflurane anaesthesia

The neuromuscular and cardiovascular effects of mivacurium chloride were studied during nitrous oxide-oxygen narcotic (fentanyl) (n = 90) and nitrous oxide-oxygen isoflurane (ISO) anaesthesia (n = 45). In addition, a separate group (n = 9) received succinylcholine during fentanyl anaesthesia to compare its neuromuscular effects with mivacurium. Mivacurium was initially administered as a single bolus in doses from 0.03 mg.kg-1 to 0.25 mg.kg-1 to study the dose-response relationships, as well as the cardiovascular effects of mivacurium. Neuromuscular block (NMB) was measured by recording the twitch response of the adductor pollicis muscle following ulnar nerve stimulation (0.15 Hz, 0.2 ms supramaximal voltage). The ED95 values for mivacurium were estimated to be 0.073 mg.kg-1 and 0.053 mg.kg-1 in the fentanyl and ISO groups respectively. The duration of block (time from injection to 95 per cent recovery) for a dose of 0.05 mg.kg-1 mivacurium was 15.3 +/- 1.0 min and 21.5 +/- 1.3 min for fentanyl and ISO anaesthesia, respectively. The recovery index (25-75 per cent) between initial bolus dose (6.1 +/- 0.5 min), repeat bolus doses (7.6 +/- 0.6 min), mivacurium infusion (6.7 +/- 0.7 min) and succinylcholine infusion (6.8 +/- 1.8 min) were not significantly different. There was minimal change in mean arterial pressure (MAP) or heart rate (HR) following bolus doses of mivacurium up to 0.15 mg.kg-1. Bolus administration of 0.20 mg.kg-1 or 0.25 mg.kg-1 of mivacurium decreased MAP from 78.2 +/- 2.5 to 64.0 +/- 3.2 mmHg (range 12-59 per cent of control) (P less than 0.05). The same doses when administered slowly over 30 sec produced minimal change in MAP or HR.     

A defasciculating dose of d-tubocurarine causes resistance to succinylcholine

Forty-four patients, ASA physical status I or II, undergoing thiamylal, fentanyl, N2O/O2 anaesthesia were studied to determine the dose-response to succinylcholine (Sch) without prior defasciculation (24 pt - Group 1), or three minutes following d-tubocurarine (dTC), 0.043 mg.kg-1 (20 pt - Group 2). The individual log dose-logit response curve for each patient was determined using a cumulative dose plus infusion technique and integrated EMG monitoring of the first dorsal interosseous muscle. The mean (+/- SEM) ED50, ED90 and ED95 values for Sch in Group 1 were 0.13 +/- 0.01, 0.19 +/- 0.01 and 0.22 +- 0.01 mg.kg-1, and in Group 2 were 0.16 +/- 0.01, 0.25 +/- 0.01 and 0.29 +/- 0.02 mg.kg-1, respectively. The mean ED values in Group 2 were significantly greater than the equivalent values in Group 1 (P less than 0.05). Compared with values in Group 1, ED values in Group 2 represented mean increases of 23, 32, and 32 per cent, respectively. These pharmacodynamic data indicate that the dose of Sch needs to be increased by 32 per cent following a defasciculating dose of dTC 3 mg.70 kg-1 (0.043 mg.kg-1).     

The neuromuscular response of infants to a continuous infusion of succinylcholine

The response of the adductor of the thumb to ulnar nerve stimulation (0.1 Hz) was evaluated during continuous infusion of succinylcholine (SCh) in 20 infants anesthetized with halothane (1%) and N2O2/O2. Train-of-four stimulation (2 Hz for 2 s) was used to differentiate between phase I and phase II block. Some infants were very resistant to the neuromuscular effects of SCh. These infants (Group 1) were younger in age, 57 +/- 15 days (mean +/- SE) and required 24.6 +/- 3.3 mg X kg-1h-1 SCh to achieve more than 90% depression of the twitch. Older infants (Group 2), 188 +/- 33 days, required significantly less (P less than 0.001) SCh (8.7 +/- 0.5 mg X kg-1h-1) to achieve the same degree of twitch suppression. Group 1 infants recovered from the effects of SCh very rapidly. After 10 mg/kg SCh, the train-of-four ratio in Group 1 infants recovered to 75% in 4.7 +/- 0.6 min, whereas it took 34 +/- 10 min in Group 2 infants (P less than 0.01). Tachyphylaxis developed in infants after 3.6 +/- 0.3 mg/kg (mean +/- SE) and phase II block after 5.3 +/- 0.7 mg/kg (P less than 0.05) SCh. Combining the data of infants with that of children from a previous study conducted in a similar fashion resulted in significant correlation (P less than 0.001) between the log age and SCh requirement. The rate of administration of a continuous infusion of SCh in infants should be based upon the response of infants and not on a fixed dose (mg X kg-1 X h-1).     

Neostigmine,pyridostigmine and edrophonium as antagonists of deep pancuronium blockade

To compare the ability of equipotent doses of neostigmine, pyridostigmine and edrophonium to antagonize intense pancuronium neuromuscular blockade, one hundred and twenty ASA physical status I or II patients scheduled for elective surgery received 0.06 mg.kg-1 pancuronium during a thiopentone nitrous oxide-enflurane anaesthetic. Train-of-four stimulation was applied every 12 s and the force of contraction of the adductor pollicis muscle was recorded. In the first 60 patients, spontaneous recovery was allowed until ten per cent of initial first twitch height. Then neostigmine (0.005, 0.01, 0.02 or 0.05 mg.kg-1), pyridostigmine (0.02, 0.04, 0.1 or 0.2 mg.kg-1), or edrophonium (0.1, 0.2, 0.4 or 1 mg.kg-1) was injected by random allocation. Dose-response relationships were established from the measurement of first twitch height (T1) ten minutes later. From these, neostigmine, 0.04 and 0.08 mg.kg-1 was found to be equipotent to pyridostigmine, 0.2 and 0.38 mg.kg-1, and edrophonium, 0.54 and 1.15 mg.kg-1, respectively. These doses were given by random allocation to the next 60 patients, but at one per cent spontaneous recovery. Neostigmine, 0.04 mg.kg-1, produced a T1 of 73 +/- 4 per cent (mean +/- SEM), and a train-of-four ratio (TOF) of 39 +/- 3 per cent. This was significantly greater than with pyridostigmine, 0.2 mg.kg-1 (T1 = 50 +/- 6 per cent; TOF = 25 +/- 3 per cent), and edrophonium, 0.54 mg.kg-1 (T1 = 54 +/- 3 per cent; TOF = 17 +/- 2 per cent).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of an intubating dose of succinylcholine and atracurium on the diaphragm and the adductor pollicis muscle in humans

This study compares the neuromuscular blocking effect of succinylcholine (0.8 mg . kg-1) and atracurium (0.6 mg.kg-1) on the diaphragm (D) and the adductor pollicis (AP) in 20 patients anesthetized with nitrous oxide, oxygen, and fentanyl. The diaphragm was monitored by measuring transdiaphragmatic pressure following bilateral phrenic nerve stimulation. After succinylcholine, the time from injection of succinylcholine to maximum depression of the single twitch response (onset time) was of 50 +/- 11 s (+/- SD) for D compared to 80 +/- 24 s for AP (P less than 0.001). After succinylcholine, recovery from paralysis was earlier for D than AP. Single twitch height (TH) returned to 25% of its control value (T25) after 5 +/- 2 min for D compared to 7 +/- 3 min for AP (P less than 0.001). Complete recovery of TH (T100) was achieved after 9 +/- 4 min for D and 11 +/- 5 min for AP (P less than 0.01). Recovery index (T25-75) was of 2 +/- 1 min for both muscles. After atracurium, the onset time for D was of 137 +/- 31 s compared to 181 +/- 45 s for AP (P less than 0.001). The T25 was achieved after 38 +/- 7 min for D compared to 63 +/- 13 min for AP (P less than 0.001). The TH of D returned to T100 after 60 +/- 12 min compared to 87 +/- 17 min for AP (P less than 0.01). The train-of-four ratio returned to 1 after 64 +/- 15 min for D compared to 99 +/- 21 min for AP (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of enflurane and fentanyl on the clinical characteristics of long-term succinylcholine infusion

The characteristics of the neuromuscular block produced by prolonged succinylcholine infusion were compared in 40 patients anaesthetized with either nitrous oxide with enflurane (1-2 per cent inspired) or nitrous oxide and fentanyl. Neuromuscular transmission was monitored using train-of-four stimulation and the infusion rate was adjusted to keep the first twitch at 10-15 per cent of its control value. Initially, all patients, exhibited a depolarizing-type block all twitches of the train-of-four being roughly the same size, and the infusion rates were similar in the enflurane (54 microgram X kg-1/min) and the fentanyl (58 microgram X kg-1/min) groups. Tachyphylaxis developed later in both groups and correlated well with the onset of phase II block (dual block). This occurred sooner and at a lower cumulative dose in the enflurane group. Fourth to first twitch ratios decreased to 50, 25 and 0 per cent in 31, 46 and 59 minutes in the enflurane group, at cumulative succinylcholine doses of 2.2, 3.2 and 4.2 mg X kg-1 respectively. Corresponding figures for the fentanyl group were 52, 73 and 86 minutes, with dose of 3.4, 5.0 and 5.9 mg X kg-1. Infusion rates increased markedly after establishment of dual block, but were similar with enflurane (0.99 mg X kg-1/min) and fentanyl (1.12 mg X kg-1/min). Ten minutes after stopping the infusion fourth to first twitch ratios failed to reach 50 per cent in most patients given enflurane who had received more than 6 mg X kg-1 succinylcholine over more than 90 minutes. Corresponding figures for fentanyl patients were 13 mg x kg-1 and 150 minutes. The block in all 15 patients (9 enflurane, 6 fentanyl) who did not recover spontaneously was successfully antagonized with atropine and neostigmine.     

Atracurium for short surgical procedures: a comparison with succinylcholine

A comparison was made between atracurium and succinylcholine in 40 patients undergoing short gynaecological procedures of 30 minutes or less. Good intubating conditions were produced in 76.7 +/- 39.3 seconds (mean +/- S.D.) with succinylcholine 1 mg . kg-1 and 198 +/- 84 seconds with atracurium 400 micrograms . kg-1. Muscle relaxation was maintained with the initial dose of atracurium or with repeated boluses of succinylcholine. The mean time of surgery was 17.65 +/- 5.3 minutes in the atracurium group and 15.2 +/- 4.6 minutes in the succinylcholine group. Residual neuromuscular block with atracurium was reversed with neostigmine 0.036 mg . kg-1 and atropine 0.018 mg . kg-1. Recovery of neuromuscular function following reversal, assessed by return of all responses to train-of-four stimulation occurred in 5.05 +/- 4.6 minutes in the atracurium group but half the above doses of neostigmine and atropine were repeated in three patients. We conclude that a single dose of atracurium 400 micrograms . kg-1 is suitable for intubation and maintainance of muscle relaxation for short surgical procedures. However, the onset of action is slow, compared to succinylcholine. Residual neuromuscular block can be antagonised with standard doses of neostigmine, less than 20 minutes after the initial dose of relaxant. Atracurium appears to be a suitable alternative for short procedures where succinylcholine is unsuitable or contraindicated.     

“Priming” with neostigmine: failure to accelerate reversal of single twitch and train-of-four responses

Train-of-four stimulation can shorten the apparent onset time of neuromuscular blocking drugs. This study was designed to verify whether the same occurred with neostigmine-assisted recovery, and whether this apparent acceleration could explain the previously reported effectiveness of the priming technique for reversal agents. Fourteen adults received atracurium, 0.5 mg.kg-1, during a thiopentone-nitrous oxide-enflurane anaesthetic. The ulnar nerves of both arms were stimulated with train-of-four stimulation every 12 seconds until 1 per cent recovery of first twitch, at which time stimulation in one arm was switched to single twitch. When mean first twitch height reached 10 per cent of control, neostigmine, 0.04 mg.kg-1, was administered either as a single bolus, or as a "priming" dose of 0.01 mg.kg-1, followed 3 min later by 0.03 mg.kg-1. No statistically significant differences were observed between single twitch in one arm and first twitch height of the train-of-four in the other arm for the next 10 min. With priming, first twitch height was 45 +/- (SEM) 5 per cent at 5 min and 85 +/- 6 per cent at 10 min, compared with 72 +/- 5 per cent (p less than 0.05) and 91 +/- 2 per cent (NS) respectively without priming. Train-of-four ratio was 28 +/- 3 per cent at 5 min and 65 +/- 5 per cent at 10 min with priming, versus 53 +/- 4 per cent (P less than 0.05) and 73 +/- 3 per cent (NS) respectively without priming.(ABSTRACT TRUNCATED AT 250 WORDS)     

Accelerated onset and delayed recovery of d-tubocurarine blockade with pancuronium in infants and children

The effect of age on the onset and duration of action of a d-tubocurarine (DTC) neuromuscular blockade with and without pancuronium priming in children was examined. Sixty ASA physical status I or II patients in three age ranges (0-1 yr, 1-3 yr and 3-10 yr) were anaesthetized with thiopentone, halothane and nitrous oxide. Each patient received either a single paralyzing dose of DTC 0.4 mg.kg-1, or DTC 0.36 mg.kg-1 preceded three minutes earlier by pancuronium 0.007 mg.kg-1. Evoked force of contraction of the adductor pollicis was measured using train-of-four stimulation applied every 12 sec. Time to 90 per cent first twitch depression after a single dose of DTC increased with increasing age (r = 0.65, p less than 0.01), and was 1.6 min (SEM +/- 0.3) in the 0-1 yr group, 1.9 +/- 0.3 min (1-3 yr), and 5.2 +/- 1.2 min (3-10 yr). Time to ten per cent spontaneous recovery after single dose DTC was shorter in older individuals (r = 0.40, p less than 0.05), being 36.4 +/- 5.1 min in infants 0-1 yr, 30.6 +/- 4.6 min (1-3 yr), and 24.0 +/- 2.7 min (3-10 yr). Priming with pancuronium accelerated the onset significantly in all age groups with 90 per cent T1 depression occurring at 0.7 +/- 0.1 min (0-1 yr), 0.9 +/- 0.1 min (1-3 yr), and 2.1 +/- 0.6 min (3-10 yr). However, priming delayed recovery, especially in infants.(ABSTRACT TRUNCATED AT 250 WORDS)     

Does vecuronium accumulate in the renal transplant patient?

Twenty ASA physical status Class III patients undergoing cadaver renal transplantation were studied. After 90 per cent T1 recovery, as determined by train-of-four measurement, from 1.0 mg.kg-1 succinylcholine to facilitate tracheal intubation, nine patients received atracurium 0.25 mg.kg-1 (Group I) and 11 patients received vecuronium 0.05 mg.kg-1 (Group II) intravenously. The following measurements were made: time to maximum block onset (first dose Max), injection to start of recovery (start REC1), injection to 25 per cent T1 twitch recovery (REC 251), injection to 75 per cent T1 (REC 75(1], injection to 90 per cent T1 (REC 90(1] and time from 25-75 per cent recovery T1 (REC 25-75(1]. Maximum blockade (Max block 1) was also measured. At 90 per cent T1 recovery, if time permitted, an identical dose of the appropriate relaxant was administered. Time from second dose to onset of maximum block (second dose Max) and 90 per cent recovery after second dose (REC 90(2] were then measured. At the conclusion of surgery, neuromuscular blockade was reversed with neostigmine 2.5 mg and glycopyrrolate 0.5 mg. One way ANOVA was performed to determine significance between the groups and a p less than 0.05 was considered significant. A paired t test was also performed between REC 90(1) and REC 90(2) for atracurium and vecuronium respectively. A p less than 0.05 was again considered significant. Measurement of first dose Max, start REC1, REC25(1), REC 75(1), REC 90(1), REC 25-75(1) and Max block 1 revealed no difference between the patients receiving an initial dose of atracurium and those receiving vecuronium.(ABSTRACT TRUNCATED AT 250 WORDS)     

Neuromuscular blockade for rapid tracheal intubation in children: comparison of succinylcholine and pancuronium

To compare the effectiveness of succinylcholine and pancuronium for rapid intubation in children, 49 healthy children ages two to eight years were studied. After induction of anaesthesia with thiopentone and atropine, and administration of droperidol, fentanyl, nitrous oxide, and oxygen, each child received one of the following muscle relaxants: succinylcholine 1.5 mg X kg-1 (n = 12), succinylcholine 1.0 mg X kg-1 (n = 13), pancuronium 0.15 mg X kg-1 (n = 11), or pancuronium 0.10 mg X kg-1 (n = 13). The force of thumb adduction was measured by stimulating the ulnar nerve with repetitive supramaximal single twitches (0.15 Hz). The time to 95 per cent twitch depression (mean +/- S.D.) was most rapid with succinylcholine 1.5 mg X kg-1 (40.8 +/- 3.0 seconds) and succinylcholine 1.0 mg X kg-1 (51.8 +/- 14.0 seconds), slowest with pancuronium 0.10 mg X kg-1 (150.9 +/- 38.0 seconds), and intermediate with pancuronium 0.15 mg X kg-1 (80.3 +/- 21.8 seconds) (p less than 0.005). The intubating conditions were excellent in 100% of the children who received succinylcholine 1.5 and 1.0 mg X kg-1, and pancuronium 0.15 mg X kg-1, but were excellent in only 69 per cent of those who received pancuronium 0.10 mg X kg-1. We conclude that succinylcholine 1.5 mg X kg-1 produces the most rapid onset of excellent intubating conditions in children. In children in whom succinylcholine is contra-indicated, pancuronium 0.15 mg X kg-1 provides excellent intubating conditions within 80 seconds.     

Postoperative neuromuscular block following atracurium or alcuronium in children

Postoperative neuromuscular block (NMB) was evaluated in 60 children who received randomly either atracurium or alcuronium to induce and maintain an 85-95 per cent NMB during balanced anaesthesia. The EMG-monitor was turned away from the anaesthetist 10-15 min before the end of surgery. The average NMB was comparable between the groups at the time of reversal with neostigmine 50 micrograms.kg-1 (84 +/- 9 per cent, mean +/- SD) as were the NMB and the train-of-four ratio when the tracheas were extubated on a clinical basis (32 +/- 20 per cent and 50 +/- 18 per cent, respectively). Patients who had been paralyzed with atracurium arrived at the recovery room earlier and on arrival had greater train-of-four ratios than the patients paralyzed with alcuronium (P less than 0.01). Time to a train-of-four ratio of greater than 90 per cent was significantly shorter in the atracurium group (10 +/- 5 min vs 26 +/- 15 min, P less than 0.001). Thus, an intermediate-acting muscle relaxant offers a safer recovery profile of the NMB than a long-acting muscle relaxant in paediatric patients.     

Accelerated reversal of atracurium blockade with divided doses of neostigmine

The hypothesis that administration of neostigmine in divided doses might accelerate the antagonism of neuromuscular blockade was investigated. Neostigmine 0.05 mg X kg-1 was administered either in a single bolus dose (Group I, n = 16) or in an initial dose of 0.01 mg X kg-1 followed three minutes later by 0.04 mg X kg-1 (Group II, n = 16) for antagonism of atracurium-induced blockade. Reversal was attempted at 10 per cent spontaneous recovery of twitch height. The mean time (+/- SD) from the first injection of the drug until the train-of-four (TOF) ratio value had reached 0.75 was significantly shorter in Group II (p less than 0.05) than in Group I (391.8 +/- 83.3 and 468.6 +/- 150.3 seconds respectively). The rate of TOF ratio recovery was 2.5 times faster after neostigmine administration in divided doses. It is concluded that administration of neostigmine in divided doses, as described in this study, produced a significantly faster reversal of residual atracurium-induced neuromuscular blockade as compared to a single bolus administration.     

Modification by ketamine on the neuromuscular actions of magnesium,vecuronium, pancuronium and alpha-bungarotoxin in the primate

The neuromuscular effects of ketamine, at cumulative doses of 2.5 and 10 mg.kg-1 iv, were studied by electromyographically quantifying the thumb response evoked by ulnar nerve stimulation in 25 monkeys anaesthetized with pentobarbital-N2O-O2. Ketamine alone at these doses had no neuromuscular effects. When the EMG response was maintained at 50% of control by a continuous infusion of magnesium, vecuronium, or pancuronium, ketamine depressed the responses by an additional 13 +/- 3%, 34 +/- 7% and 32.5 +/- 3.3% (mean +/- SEM), respectively, at the highest dose, P less than 0.05. In contrast, ketamine had no effect on the neuromuscular block produced by incremental doses of alpha-bungarotoxin. These results indicate that ketamine does not act on the postjunctional acetylcholine receptor. It plays a secondary role in neuromuscular block, possibly by prejunctional or postjunctional effects independent of receptor occupation.     

Comparison of the effects of succinylcholine and atracurium on intracranial pressure in monkeys with intracranial hypertension

The effects of succinylcholine (1.5 mg X kg-1 IV) administered five minutes after a defasciculating dose of curare (0.05 mg X kg-1 IV), were compared with the effects of atracurium (0.5 mg X kg-1 IV) on intracranial pressure (ICP) in 13 cynomolgus monkeys with intracranial hypertension (ICP approximately 25 mmHg). Neither succinylcholine nor atracurium increased ICP during general anaesthesia with 60 per cent N2O/O2, 0.5-1 per cent halothane. During a rapid sequence induction and intubation with thiopentone 5 mg X kg-1 IV, ICP increased equally with intubation following both atracurium (25 +/- 1 to 32 +/- 2 mmHg) and succinylcholine (25 +/- 1 to 31 +/- 2 mmHg) (p less than 0.05). Intubation was also associated with significant increases in PaCO2, CVP and MAP. We conclude that in this primate model of intracranial hypertension, neither atracurium nor succinylcholine (when given following a defasciculating dose of curare) elevates ICP. In terms of the elevation of ICP associated with intubation, atracurium was found to offer no advantage over succinylcholine.     

Onset of neuromuscular block at the masseter and adductor pollicis muscles following rocuronium or succinylcholine

PURPOSE: To compare the onset time of two different rocuronium doses (0.6 and 0.9 mg x kg(-1)) and succinylcholine (1.5 mg x kg(-1), preceeded by 0.06 mg x kg(-1) rocuronium) at the masseter and the adductor pollicis muscle. METHODS: In a randomized study, 60 ASA I or II adult women, 18-65 yr of age, were anesthetized with propofol and fentanyl and nitrous oxide in oxygen. Neuromuscular monitoring was performed using acceleromyography simultaneously on the masseter and adductor pollicis. Onset time was measured at both muscles using supramaximal 0.1 Hz single twitch stimulation (square-wave pulse 0.2 msec duration). RESULTS: In all patients, complete neuromuscular block occurred at the masseter and adductor pollicis muscles. Lag-time and onset time were faster at the masseter that at the adductor pollicis muscle in both rocuronium-groups (P < 0.01) and in the succinylcholine-group (P < 0.01). Furthermore, onset time was more rapid after 0.9 mg x kg(-1) rocuronium (65 +/- 7 s) than after succinylcholine (83 +/- 19 sec) at the AP (P < 0.05), but did not differ at the masseter (33 +/- 6 vs 36 +/- 7 sec). CONCLUSIONS: Following rocuronium and succinylcholine, onset time is faster at the masseter than at the adductor pollicis muscle.     

Pancuronium increases the duration of electroencephalogram burst suppression in dogs anesthetized with isoflurane.

Earlier studies have demonstrated both a decrease as well as no effect on halothane MAC after administration of nondepolarizing neuromuscular relaxants. To clarify further the relationship between neuromuscular blocking agents and anesthetic potency, the authors studied the effect of pancuronium on steady-state electroencephalogram (EEG) burst suppression produced by isoflurane in dogs. Anesthesia was induced using isoflurane and oxygen via mask without the administration of other drugs. The trachea was intubated, and isoflurane was administered at a concentration sufficient to produce EEG burst suppression. Thereafter, end-tidal isoflurane concentration, temperature, and end-tidal PCO2 were meticulously maintained at constant values. Dogs in group 1 (n = 6) received pancuronium 0.1 mg.kg-1. The percent of the EEG that was isoelectric increased from 21 +/- 9% (mean +/- SD) to 35 +/- 11% (P less than 0.01). After the return of single-twitch response to train-of-four stimulation, neostigmine 0.05 mg.kg-1 and glycopyrrolate 0.01 mg.kg-1 were administered. This resulted in a reduction in EEG isoelectricity to 19 +/- 8% (P less than 0.01), similar to the value before pancuronium administration. In group 2 dogs (n = 6), the percent isoelectricity of the EEG prior to pancuronium was 25 +/- 10%. After administration of pancuronium 0.02, 0.04, and 0.2 mg.kg-1 sequentially, the percent isoelectricity of the EEG was 29 +/- 11, 37 +/- 15, and 43 +/- 9%, respectively. This represents a dose-related increase in isoelectricity for the 0.04- and 0.2-mg.kg-1 doses (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Onset of pancuronium and d-tubocurarine blockade with priming

The synergistic effect of pancuronium bromide (PCB) and d-tubocurarine (DTC) on the onset time of neuromuscular blockade was tested in 108 ASA physical status I and II adults anaesthetized with thiopentone, nitrous oxide and halothane. Either saline or a small (priming) dose (DTC, 0.04 mg X kg-1, or PCB, 0.007 mg X kg-1) was administered 3 min before a paralyzing dose of either DTC or PCB. The total dose of relaxant was equivalent to DTC, 0.4 mg X kg-1, or PCB, 0.07 mg X kg-1. Neuromuscular activity was measured using train-of-four stimulation applied every 12 s. Time to 50 per cent first twitch blockade was 63 +/- 4.6 s (mean +/- SEM) with DTC and 88 +/- 5.2 s with PCB (p less than 0.002). Times to 90 per cent blockade were not different between the two drugs (161 +/- 20 s and 141 +/- 21 s respectively). Priming a DTC blockade with either DTC or PCB or priming a PCB blockade with PCB produced an acceleration of less than 10 s at all levels of blockade. Compared with PCB alone, priming PCB blockade with DTC reduced the time to 50 per cent blockade to 71 +/- 4.5 s (p less than 0.02) and to 90 per cent blockade to 111 +/- 8 s (p less than 0.05). Priming did not affect the duration of action significantly, except in the case of PCB priming of DTC, where duration was increased from 39 +/- 4.4 to 57 +/- 4 min (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of cimetidine on neuromuscular blockade by succinylcholine and pancuronium

The effect of cimetidine on neuromuscular blockade by succinylcholine and pancuronium was investigated in 54 adult patients scheduled for elective surgery. The neuromuscular blocking properties were estimated with single twitch height (T1) which was obtained by measuring the acceleration of adduction of the thumb in response to the ulnar nerve stimulation under N2O-fentanyl anesthesia. In cimetidine group, cimetidine 200 mg was administered orally on the night before surgery and 90 mins before anesthesia. Succinylcholine 1 mg.kg-1 (n = 14) or 1.5 mg.kg-1 (n = 20) was injected intravenously, and the onset time (from injection to 0% T1), the duration of maximal block (0% T1), and the recovery time from injection to 50% and 75% of control twitch height were evaluated. ED25 and ED50 of pancuronium were calculated from the dose response curve obtained by incremental administration of the drug (n = 20) whose total cumulative dose was 0.1 mg.kg-1. The recovery index of pancuronium was determined by measuring the 25%-75% recovery time. There was no significant difference between cimetidine pretreated patients and non-pretreated patients regarding these parameters of neuromuscular blockade with both succinylcholine and pancuronium. In conclusion, cimetidine has no influence on neuromuscular blockade of succinylcholine and pancuronium under N2O-fentanyl anesthesia.     

Increases in intracranial pressure from succinylcholine: prevention by prior nondepolarizing blockade

Whether succinylcholine causes an increase in intracranial pressure (ICP) in patients with brain lesions is uncertain and, if increased ICP does occur, its pathophysiology remains unknown. The authors investigated both the effect of succinylcholine on ICP and its modification with prior neuromuscular blockade by measuring ICP (subarachnoid bolt) in 13 consecutive patients with brain tumors who received succinylcholine both before and after complete neuromuscular blockade with vecuronium. Anesthesia was induced with thiopental, 6 mg X kg-1 iv, and nitrous oxide, 70% in oxygen, while ventilation was controlled (PaCO2 = 37.2 mmHg +/- 1.7 SE). Succinylcholine, 1 mg X kg-1 iv, was administered and ICP, heart rate (HR), and blood pressure (BP) were recorded until normal twitch tension was restored. Complete neuromuscular blockade was then established with vecuronium, 0.14 mg X kg-1 iv; 3 min later, succinylcholine, 1 mg X kg-1 iv, was repeated. The resulting changes in ICP, HR, and BP were recorded for 3 min. Following the first dose of succinylcholine, mean ICP increased from 15.2 mmHg +/- 1.3 SE to 20.1 mmHg +/- 2.0 SE (P less than 0.05), with five of the patients sustaining increases in ICP of 9 mmHg or greater. In contrast, when succinylcholine was given after vecuronium-induced paralysis, no patient developed an increase in ICP greater than 3 mmHg (P less than 0.05 compared with the incidence of ICP greater than or equal to 9 mmHg observed after the first dose of succinylcholine). A second group of six patients received two doses of succinylcholine according to the same protocol but without an intervening dose of vecuronium.(ABSTRACT TRUNCATED AT 250 WORDS)