ANAESTHESIA With the steroid agent Althesin is usually associated with reductions in arterial blood pressure. 1-7Depending on the rate of iniection, the maximum depressant effect on blood pressure occurs usually after two or three minutes, while recovery requires approximately 15 minutes. 8 The hypotension has been attributed to a reduction in peripheral resistance 4,6,'9 since cardiac output remains unaltered. 8,1~ Although myocardial contractility 11 and stroke volume 4,1~ are depressed, cardiac output remains constant due to a concomitant increase in heart rate. 8,5,r,l~ Large doses of Althesin prevent the reflex bradycadia in response to the pressor effect of adrenaline, suggesting that the baroreceptor reflex is impaired? 4 As the pressor effects of adrenaline TM and methoxamine a are unaffected by the drug, its action is unlikely to be a direct one on vascular smooth muscle.We have investigated the effects of Althesin on central sympathetic discharge and baroreceptor pathways, to clarify their influence on the circulatory responses observed.
METHODSMale New Zealand white rabbits weighing 2.8 to 3.5 kg were anaesthetized with pentobarbitone, or were decerebrated. The latter procedure was carried out under anaesthesia with 3 per cent halothane in oxygen, following early insertion of a tracheal cannula. The accompanying arterial pressure drop restricted bleeding and rendered carotid clamping unnecessary. At least one hour was allowed to elapse after administration of halothane had been discontinued before the effects of Althesin or thiopentone were studied.In intact rabbits anaesthesia was induced with pentobarbitone 30 mg/kg given initially through the marginal ear vein, subsequent maintenance doses of 4 mg/kg being administered every 40 minutes through a femoral vein cannula.Following the preparatory period, gallamine 1 mg/kg was given intravenously every 40 minutes in all animals. Mechanical ventilation using a Harvard pump Model 613 with 100 per cent oxygen was adjusted to maintain end-tidal carbon dioxide at approximately 4 per cent as monitored with a Beckman LB-2 carbon dioxide analyzer. Arterial pressure was recorded from the femoral artery with a Bell and Howell transducer, and heart rate was obtained from the pressure channel by means of a Devices instantaneous ratemeter. These measurements were