Cerebral circulatory and metabolic effects of hypotension produced by deep halothane anaesthesia.
Hypotension to a mean blood pressure of 33 mmHg for periods of 70 to 187 minutes was induced by increasing the inspired halothane concentration in 11 baboons which were already anaesthetized with 0·5% halothane, nitrous oxide, and oxygen. During hypotension, cerebral blood flow, measured by Xenon clearance and by a carotid electromagnetic flowmeter, decreased by more than half, and sagittal sinus oxygen saturation was 46%. Cerebral oxygen uptake fell from 5·15 to 3·56 ml./100 g/min at this deeper level of halothane anaesthesia. Cerebral hyperaemia developed after hypotension in those animals which regained a mean blood pressure greater than 70 mmHg. Acidbase measurements on CSF from the cisterna magna revealed no metabolic acidosis during or after hypotension. In all four animals with intact autoregulation before hypotension, this was absent or impaired afterwards.
D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000378:metabolism; D000769:Anesthesia, Inhalation; D000818:Animals; D001794:Blood Pressure; D001921:Brain / Q000378:metabolism*; D002245:Carbon Dioxide / Q000097:blood; D002560:Cerebrovascular Circulation; D004569:Electroencephalography; D006221:Halothane; D000882:Haplorhini; D006863:Hydrogen-Ion Concentration; D007023:Hypotension, Controlled; D007427:Intracranial Pressure; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D010215:Papio; D010313:Partial Pressure; D014655:Vascular Resistance; D014978:Xenon
D002245:Carbon Dioxide; D014978:Xenon; D010100:Oxygen; D006221:Halothane