No abstract

Previous investigation suggests that the degree of sympatho-adrenal activity which a particular anaesthetic evokes may help to explain many of its pharmacological effects. For example, during the inhalation of halothane, peripheral vasodilatation is probably associated with sympathetic suppression, whereas vasoconstriction and increased sympathetic activation appear to be characteristic of cyclopropane anaesthesia 1'2.Ether is often used as a basis for evaluating newer inhalational anaesthetics and it was considered to be of some importance to determine whether a relationship exists between certain circulatory, respiratory, metabolic and pupillary effects of this agent and plasma adrenaline and noradrenaline concentrations. M E T H O D SEleven healthy female subjects, aged from 23 to 56 years and about to undergo minor surgical procedures, were studied. All pre-anaesthetic medication was omitted. Anaesthesia was induced with thiopentone (4mg/kg) and maintained with nitrous oxide and oxygen (25 per cent), using a non-rebreathing system incorporating a Ruben valve.Initial measurements were made during this control period which lasted for twenty to thirty minutes. Increasing concentrations of ether were then added to the nitrous oxide and oxygen mixture from an EMO vaporiser until a stable state of anaesthesia with 15 per cent vapour strength had been attained for thirty minutes. In five of the subjects data were also collected during ten minute periods of 5 per cent and 10 per cent ether anaesthesia.Arterial pressures was measured by the auscultatory method in nine of

Limb blood flow was studied in twelve subjects, during trichloroethylene anaesthesia, using venous occlusion plethysmography. There was no significant alteration in blood flow or vascular resistance in the series as a whole. In some cases there was evidence of peripheral vasodilatation which was not abolished by nerve block. This was associated with tachypnoea and it was considered to be the result of the action of trichloroethylene on the blood vessel wall. Vasodilatation during trichloroethylene anaesthesia was replaced by vasoconstriction when the tachypnoea was abolished by means of intravenous pethidine. It is suggested that this is a compensatory vasoconstriction in response to a fall in the cardiac output, brought about by the combined effects of the narcotic and the anaesthetic agent.

In nine patients, with preoperative ICP monitoring, anaesthesia was induced with thiopentone 5 mg kg-1 given over 1 min, followed by pancuronium 0.1 mg kg-1. After manual hyperventilation with nitrous oxide and oxygen for 3 min they were given thiopentone 2.5 mg kg-1 over 30 s (phase 1); 30 s later laryngoscopy was performed and topical analgesia administered to the larynx. Endotracheal intubation was performed 1 min after spraying the cords (phase 2). The measurements continued for a further 5 min during which the patients were mechanically ventilated (phase 3). ICP and intra-arterial pressure were recorded. Although there was a significant decrease (P less than 0.05) in MAP at the end of the second dose of thiopentone, there were no other significant changes in ICP, MAP or PaCO2 throughout the study. In two patients there were transient decreases in cerebral perfusion pressure to less than 60 mm Hg. Although MAP increased in five of the patients during laryngoscopy and intubation, there was no increase in ICP, showing that the MAP was still within the autoregulatory limits.