We have assessed intubating conditions after administration of Org 9426 (rocuronium) 600 micrograms kg-1 at 60 or 90 s in groups of 20 patients anaesthetized with thiopentone, nitrous oxide in oxygen and small doses of fentanyl, and compared the data with those obtained after suxamethonium 1 mg kg-1 in similar groups of patients. The influence of prior suxamethonium administration on the potency of Org 9426 was studied also by constructing a dose-response curve. Intubating conditions after Org 9426 were found to be clinically acceptable (good or excellent) in 95% of patients at 60 s and in all patients at 90 s and in all patients at both times after suxamethonium. The average time for the onset of block following Org 9426 at this dose was 89 s (which is shorter than with any of the currently available non-depolarizing neuromuscular blocking drugs); the duration of clinical relaxation (25% recovery of twitch height) 30 min. Prior administration of suxamethonium did not appear to influence the potency of Org 9426.

We gave either midazolam or propofol for induction of anaesthesia to 140 ASA I or II female patients (18-60 yr). ED50 values were obtained by probit analysis for three clinical end-points: loss of response to command; loss of eyelash reflex; failure to respond to application of an anaesthetic face mask delivering 1% isoflurane. Propofol ED50 values (95% confidence intervals) were 1.25 (0.99-1.48) mg kg-1, 1.61 (1.29-1.94) mg kg-1 and 1.51 (1.20-1.82) mg kg-1, respectively. ED50 values for midazolam were 0.26 (0.20-0.37) mg kg-1, 0.29 (0.23-0.47) mg kg-1 and 0.25 (0.20-0.32) mg kg-1, respectively. An additional 92 similar patients received one of nine dose combinations of midazolam and propofol for induction of anaesthesia, propofol being administered 2 min after midazolam. Success of induction was based on the clinical end-point of loss of response to command. Administration of 25% of the ED50 of midazolam followed by 50% of the ED50 of propofol resulted in loss of response to command in 50% of patients, while 50% of the ED50 of midazolam, followed by 25% of the ED50 of propofol had the same effect. A probit regression model specifying a synergistic interaction between midazolam and propofol fitted the data significantly better than a model specifying no interaction.

The use of di-isopropyl phenol (Diprivan) for induction of anaesthesia was assessed in doses ranging from 1 to 3 mg kg-1. With less than 1.75mg kg-1 not all patients were anaesthetized; 2.0 mg kg-1 appeared to be a satisfactory induction dose. Involuntary muscle movement, cough and hiccup at induction were rare with any dose studied. However, the frequency of hypotension and respiratory depression were related to the dose given. Pain on injection was uncommon when the drug was given into an antecubital vein, but occurred in 39% of patients when injected to the back of the hand or wrist. Recovery was rapid, and characterized by lack of emetic sequelae. Di-isopropyl phenol 1.5 - 2.0 mg kg-1 given rapidly during reactive hyperaemia can produce anaesthesia in one arm-brain circulation time. A reaction involving flush, hypotension, cough, laryngospasm and bronchospasm occurred in one patient receiving 2.5 mg kg-1 given over 20 s.

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The plasma cortisol level of patients anaesthetized for 1 hour with thiopentone and nitrous oxide was found to remain unchanged. During body surface surgery it rose slightly, and during intra-abdominal surgery it rose to more thap double the resting value. The blood sugar under the same circumstances changed in a qualitatively similar manner and the free fatty acids appeared to fall during anaesthesia without surgery, changed litde during body surface surgery, and rose during intra-abdominal surgery. Plasma insulin during both types of surgery showed no significant change.