SummaryThe ef'ective dose qj' thiopentone in 90% (ED,,) of unpremedicated children is 10.5 mglkg. This is significantly greater (p < 0.01) than in premedicated children. The ED,, in children premedicated with TDP ( a mixture of trimeprazine, droperidol and physeptone with atropine) is 4.2 mglkg which is significantly less (p < 0.05) than with trimeprazine and atropine (ED,, 5.2 mglkg) or papaveretum and hyoscine (EDpo 5.0 mglkg). Key wordsInduction; anaesthesia. Premedication.It has been known for some time that premedication affects the induction dose of thiopentone in There is little information on the effect of premedication on the dose requirement of thiopentone in children although recent work indicates that children require less thiopentone than adults for induction of anae~thesia.~ Beeby and Morgan Hughes4 have shown that the frequency of satisfactory behaviour in unpremedicated children is similar to that in published trials of sedative premedication, using the same method of assessment., It is becoming fashionable to encourage the presence of a parent in the anaesthetic room. Many anaesthetists now prefer to anaesthetise unpremedicated children accompanied by a parent particularly as more day case surgery is done. The aim of this study was to compare the effect of different premedicants on the dose requirement of thiopentone and to determine the ED,, and ED,, for thiopentone with and without premedication. MethodObservations were made on 490 mentally normal children aged 1-12 years in the American Society of Anesthesiologists Physical Status grades 1-2. Children with needle phobia were excluded. There were four groups for premedication: trimeprazine 3 mg/kg and atropine 0.03 mg/kg orally I f hours pre-operatively (group I); T D P (trimeprazine 6 mg, droperidol 0.6 mg and physeptone 0.32 mg per ml) 0.25 ml/kg arid atropine 0.03 mg/kg orally 1+ hours preBarbara B

The total haemolytic complement (CH50), the complement components C3 and C4, the complement breakdown product C3d, alternative pathway activation and transferrin, were measured before, during and after cardiopulmonary bypass. As expected, CH50 decreased after heparinization, remained low during bypass and decreased further up to 8 h after bypass. C3 and C4 decreased significantly during bypass, continued to decrease for a further 8 h after bypass (by 35% and 40% respectively) and thereafter increased gradually up to 48 h. Although the depletions observed were suggestive of complement activation, there were no demonstrable increases in C3d, and in all patients the concentration of C3d remained within the normal range. Hence it was concluded that complement depletions of this magnitude were unlikely to result from complement activation. Non-specific changes in protein concentrations during bypass, as a result of dilution, redistribution or other unidentified factors, are more probable causes of the observed reductions. The acute phase response to surgery may be a factor in the subsequent increase in C3 and C4 which is seen 24 h after bypass. As transferrin concentrations in the plasma are known to decrease during this response the observed decrease in transferrin concentration would support this view.