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Equipotent, paralysing doses of pancuronium and tubocurarine were administered to 40 patients, aged from 1 day to 12 months, during nitrous oxide, oxygen and fentanyl anaesthesia. Neuromuscular activity was measured during onset and recovery from paralysis using train-of-four stimulation. At the same depression of the first stimulus of the train, the train-of-four ratio was decreased more during recovery than during onset with each drug and more with tubocurarine than with pancuronium. These resuhs are qualitatively simi1ar to those found in adults, but the decrease in train-of-four ratio was less in infants. Thus, it is concluded that prejunctional neuromuscular activity, recognized as fade in response to train-of-four stimulation, can be detected after administration of pancuronium or tubocurarine to infants, but that it is less marked than in adults.

Suxamethonium increases neuromuscular block produced by non-depolarizing agents administered subsequently. To determine if this effect has a pharmacokinetic or pharmacodynamic origin, 18 ASA physical status I or II adults received atracurium 0.2 mg kg−1, with (n = 10) or without (n = 8) previous injection of suxamethonium 1 mg kg−1, during a thiopentone—nitrous oxide—isoflurane (0.5% end-tidal) anaesthetic. Arterial blood samples were obtained and plasma atracurium concentration measured by HPLC. Train-of-four stimulation was applied to the ulnar nerve and the force of contraction of the adductor pollicis muscle was recorded. Mean (SEM) volume of distribution was slightly greater with previous suxamethonium (143 (13) ml kg−1) than without (109 (5) ml kg−1) (P < 0.04). Mean elimination half-life was unaffected (20.3 (0.8) min and 20.4 (1.6) min, respectively). Neuromuscular block was more intense and recovery was slower with previous administration of suxamethonium. Atracurium concentration at 50% block (Cp2350) was 305 (30) ng ml−1 with and 454 (25) ng ml−1 without previous suxamethonium (P < 0.01). It is concluded that suxamethonium may be associated with a slight increase in the volume of distribution of atracurium, but this effect is more than compensated by a decrease in atracurium concentration required for a given effect.

The neuromuscular blockade produced by a prolonged (> 90 min) continuous infusion of suxamethonium and measured with train-of-four stimulation was studied in 20 infants and 20 children during nitrous oxide and halothane in oxygen anaesthesia. The results were compared with a previous study in adults. Suxamethonium requirement was increased in infants and children. Mean peak infusion rates were 297 and 284 μg kg−1 min−1 in infants and children, compared with 134 μg kg−1 min−1 in adults. An initial tachyphylaxis was followed by bradyphylaxis, and the peak requirement occurred earlier in infants than in children and adults (40 v. 80–100 min). Phase II block developed during the tachyphylaxis. Recovery of neuromuscular activity commenced after stopping the infusion and was accelerated with neostigmine.

To determine the influence of enflurane on the ability of edrophonium to antagonize atracurium block, dose—response curves were constructed for edrophonium in the presence of 0%, 1% and 2% enflurane, and for 2% enflurane discontinued at the time of administration of edrophonium. One hundred ASA Physical Status I or II patients (four groups of 25), selected randomly and undergoing elective surgery, received atracurium 0.5 mg kg−1, with thio-pentone, nitrous oxide and enflurane. Supplementary doses of fentanyl were given if needed. Train-of-four (TOF) stimulation was applied every 12 s, and the force of contraction of the adductor pollicis muscle was recorded. When first twitch height (T1) had recovered spontaneously to 10 % of initial value, edrophonium 0.1, 0.2, 0.4 or 1 mg kg−1 was administered by random allocation. Enflurane concentrations remained constant, except that enflurane was discontinued in 50% of the patients who had received 2% enflurane. Monitoring was continued for at least 10 min, at which time T1 and TOF ratio (T4/T1) were measured. The ED80 for T1 recovery depended on the dose of enflurane: 0.08 (SEM 0.03), 0.21 (0.06) and 0.42 (0.18) mg kg−1 for 0%, 1% and 2% enflurane, respectively (P < 0.005). With enflurane 2% discontinued, the ED80 was 0.095 (0.050) mg kg−1 (P < 0.02 compared with 2% enflurane). The ED50 for TOF responses were 0.13 (0.05), 0.46 (0.10) and 1.04 (0.38) mg kg−1 for 0%, 1% and 2% enflurane, respectively (P < 0.001). With 2% enflurane discontinued, the ED50 for TOF was 0.17 (0.12) mg kg−1 (P < 0.05 compared with 2% enflurane). It is concluded that, even when given at the same degree of spontaneous recovery, the effect of edrophonium is markedly attenuated by enflurane.

We have studied the effect of prior administration of non-depolarizing neuromuscular blocking drugs on suxamethonium-induced increases in masseter muscle tension in 21 children aged 3–10 yr, anaesthetized with nitrous oxide and halothane using supramaximal stimulation of the ulnar nerve and the nerve to masseter. Resting tension and isometric force of contraction were measured in the adductor pollicis and masseter muscles. A sub-paralysing dose of tubocurarine 0.05 mg kg−1, a paralysing dose of atracurium 0.5 mg kg−1 or saline was given, followed 3 min later by suxamethonium 1 mg kg−1. Onset times of suxamethonium and atracurium block were shorter in the masseter than in the adductor pollicis muscle. When preceded by a sub-paralysing dose of tubocurarine, suxamethonium produced an increase in masseter tension (47 (SEM 15) g) similar to that produced by suxamethonium alone (59 (13) g). Prior administration of a paralysing dose of atracurium almost abolished this increase in tension (2.5 (2.5) g) (P < 0.05 vs saline). The tension increase in adductor pollicis was 0, 3.2 (2.2) and 5.9 (1.1) g in the atracurium, tubocurarine and saline groups, respectively. Tubocurarine and atracurium prevented muscle fasciculations in all patients. It was concluded that increased muscle tone is a normal response to suxamethonium and is greater in the masseter than adductor pollicis. Sub-paralysing doses of non-depolarizing neuro-muscular blockers have little effect, in contrast with paralysing doses. This suggests that the effect is mediated via postsynaptic receptors.

Train-of-four stimulation was applied to the ulnar and phrenic nerves in 18 adult patients anaesthetized with nitrous oxide and halothane in oxygen. The response of the adductor pollicis and the diaphragm were measured. Incremental doses of atracurium and vecuronium were given, with an infusion to replace drug lost by elimination or distribution. The mean (SEM) doses of atracurium associated with 50% and 90% depression of response to the first stimulation in the train-of-four (ED50 and ED90) were 90 (9) and 133 (10) μg kg−1 at the adductor pollicis, and 130 (9) and 245 (17) μg kg−1 at the diaphragm, respectively. The mean (SEM) ED50 and ED90 of vecuronium were 25 (2) and 38 (4) μg kg−1 at the adductor pollicis and 34 (3) and 58 (5) μg kg−1 at the diaphragm, respectively. The mean (SEM) ED50 ratios were 1.56 (0.16) for atracurium and 1.47 (0.16) for vecuronium. ED90 ratios were 1.93 (0.29) and 1.55 (0.17) for atracurium and vecuronium, respectively. It is concluded that both atracurium and vecuronium exhibit a similar degree of sparing of the diaphragm.

The anaesthetic management and postoperative complications of 110 grossly obese patients undergoing weight-reducing surgery have been reviewed. The major problems were technical, related to the bulk of the patient, and respiratory, caused by alterations in pulmonary physiology. Extradural catheters were placed in 70 patients before induction of general anaesthesia. In all patients the trachea was intubated during anaesthesia and the lungs ventilated with large tidal volumes and appropriate inspired oxygen concentrations. Muscle relaxation was achieved with extradural block in 35 patients; the remainder received pancuronium i.v. Extradural analgesia with bupivacaine provided excellent analgesia after surgery and greatly facilitated nursing care.

The effects of positive and negative and expiratory pressure on renal function have been studied in adult greyhounds with a normal blood volume and without evidence of cardiorespiratory disease. Positive expiratory pressure (+10 cm H2O) resulted in a decrease of urine volume, glomerular filtration rate and renal blood flow which returned towards normal following removal of the positive pressure. Negative expiratory pressure ( − 6 cm H2O) resulted in opposite changes in renal function.

Single twitch and train-of-four stuimulation were applied at 0.08 Hz to each ulnar nerve and the force of contraction of the adductor pollicis was recorded during onset of and recovery from neuromuscular blockade by suxamethonium 1mg kg−1 or atracuirm 0.4 mg kg−1. Times to 90% first twitch blockade of train-of-four were (mean ± SEM) 0.82 ± 0.08 and 1.98 ± 0.18 min for suxmaethonium and atracurium, respectively, compared with times to 90% single twitch blockade of 1.00±0.07 and 3.35 ± 0.37 min, respectively (p < 0.05 in both cases). Apparent onset time also depended on how long train-of-four stimulation had been applied before injection of atracurium. The mode of stimulation had little effect on time to 10% recovery. The results are consitent with stimulation-induced augmentation in muscle blood flow, which increased delivery of the drug to the neuromuscular junction.

We have compared the rates of recovery of pancuronium-induced neuromuscular blockade after administration of neostigmine during anaesthesia maintained with nitrous oxide and intermittent narcotics, halothane or enflurane. Thirty patients were studied m whom anaesthesia was maintained with 70% nitrous oxide in oxygen with: fentanyl or thiopentone, halothane (0.55–0.65% end-tidal), or enflurane (1.3–1.4% end-tidal). Muscle twitch response was measured using train-of-four stimulation. Pancuronium 3mg/70kg was antagonized with neostigmine 2.5mg/70kg at 10% spontaneous recovery of the first twitch of the train compared with control. There were no significant differences between the times to 10% spontaneous recovery of the first twitch or the rates of train-of-four recovery after neostigmine when the narcotic and halothane groups were compared. However, enflurane anaesthesia, m comparison with fentanyl, was associated with a significant increase in the time to 10% recovery (57.9 ±6.0 min v. 35.4 ±7 0 min) and with decreases in the train-of-four recoveries at 4, 5, 10, 20 and 30 min after neostigmine. We conclude that, under the conditions of this study, the antagonism of pancuronium-induced neuromuscular blockade with neostigmine was impaired during enflurane but not halothane anaesthesia.

Neuromuscular transmission was measured using train-of-four stimulation, during and after anaesthesia, in 20 patients with end-stage renal failure. Neuromuscular blockade was provided with pancuronium in single doses of either 3 or 6mg per 70 kg, and antagonized at 10% recovery with atropinc and neostigmine 25mg per 70 kg. Reversal was followed by progressive recovery of muscle twitch in every patient during the 3 h of the study. Recovery was more rapid after the smaller dose of pancuronium and was inversely correlated with the duration of blockade. It is concluded that, when pancuronium is antagonized with neostigmine in patients with renal failure, neuromuscular transmission recovers without evidence of recurarization. However, when large doses of pancuronium are antagonized with neostigmine 2 5 mg, recovery may be insufficient to ensure normal ventilatory function

The neuromuscular blockade produced by a prolonged infusion of suxamethonium was studied using train-of-four stimulation in 40 patients receiving either halothane-nitrous oxide or fentanyl-nitrous oiide anaesthesia. Initially, a depolarizing (phase I) block was observed in all patients followed by phase II block which was associated with tachyphylaxis to suxamethonium; the latter changes occurring more rapidly in the halothane group. Infusions were continued for more than 150 min in 17 patients and there was a late decrease in suxamethonium requirement in those who received halothane, but not fentanyl. Ten minutes after the suxamethonium infusion was stopped, most patients received neostigmine which was followed by rapid recovery of neuromuscular transmission.

Arterial blood samples were taken at hourly intervals for three hours from ten patients who were artificially ventilated in the immediate postoperative period following mitral valve replacement. Constant minute volume ventilation was used without periodic hyperinflation. Over the three-hour period the arterial blood oxygen tension rose slightly. It was concluded that constant volume ventilation was not associated with a progressive fall in the arterial blood oxygen tension in these circumstances.