SYNOPSISThe effect of graded, progressive hypotensioni on the autoregulation of cerebral blood flow was studied in anaesthetised baboons. Progressive hypotension was produced over a period of four to five hours, either by graded haemorrhage or by the administration of increasing concentrations of hypotensive drugs. During haemorrhagic hypotension autoregulation was maintained until the mean arterial pressure had decreased to 65% of its baseline value, below which cerebral blood flow was pressure passive. In those animals subjected to drug-induced hypotension, autoregulation persisted to lower levels of mean arterial pressure (35-40% of baseline). It is postulated that under conditions of haemorrhagic hypotension, constriction of the extraparenchymal cerebral vessels in response to sympathetic stimulation decreases the possible range ofautoregulation in the anaesthetised baboon.Since its introduction into anaesthetic and surgical practice (Gardner, 1946), controlled hypotension has been used extensively to reduce bleeding and to facilitate surgery. However, despite the widespread use of the technique, the indications for induced hypotension have not been defined clearly and considerable disagreement exists regarding its safety (Davison, 1958;Enderby, 1958; Mayrhofer, 1971). The primary objections stem from uncertainties regarding the adequacy of cerebral tissue perfusion during the period of lowered arterial pressure (Brierley and Cooper, 1962;Adams et al., 1966).The present investigations were undertaken to measure the effect of a graded and progressive decrease in systemic arterial pressure on the cerebral blood flow of anaesthetised baboons and to compare the effects of haemorrhagic and pharmacologically-induced hypotension.
METHODSYoung adult baboons (9-14 kg) were tranquillised with phencyclidine (12 mg intramuscularly) and then anaesthetised with thiopentone (7.5 mg/kg intravenously), nitrous oxide and oxygen (70%:30%). In addition, half-hourly doses of phencyclidine (2 mg intramuscularly) and suxamethonium (100 mg intiamuscularly) were administered to prevent awareness and to produce muscular relaxation. The trachea was intubated and ventilation was controlled throughout each investigation (Starling respiratory pump), the minute volume and the inspired oxygen concentration being adjusted to produce normocapnia and normoxia. The end-tidal carbon dioxide concentration was monitored continuously by an infra-red analyser (URAS 4: Hartmann and Braun). During each determination of cerebral blood flow, the arterial pH and blood-gas tensions were measured using appropriate, suitably calibrated electrodes (Radiometer). Body temperature was maintained within normal limits (36°C-38°C) by means of heating lamps. Correction was made, where necessary, for any temperature difference existing between the animal and the electrode system (Severinghaus, 1966).Cerebral blood flow was determined by external scintillation counting over the right parietal area after 014 Protected by copyright. on 11 May 2018 by guest.