This study was done to evaluate cerebral oxygenation in dogs under general anaesthesia with combined hypervenlilation and hypotension. Cerebral and muscle oxygen tensions, cerebrospinal fluid lactate, pyruvate, and creatine phosphokinase (CPK) were measured to test for cerebral hypoxia.Twenty dogs were anaesthetized with thiopentone 5 rag. kg -t and their tracheae were intubated. Anaesthesia was maintained with nitrous oxide and oxygen (50150), halothane 0.5 per cent, pancuronium 0. I mg. kg -~ per 1-2 hours and ventilation was controlled. Five dogs were maintained at normocapnia and normotension, five dogs were hyperventilated to Pa{,o~ 3.33 kPa (25 mm Hg) while blood pressure was kept at baseline levels (hyperventilation alone), and 10 dogs were hyperventilated to Paco~ 3.33 kPa (25 mm Hg) followed by deliberate hypotension to a mean arterial pressure of 6.65 kPa (50 mm Hg) with the use of nitroprusside and halothane (combined hyperventilation and hypotension).Cerebrospinal fluid lactate increased significantly from control during hyperventilation alone, with an even greater increase to above 4 mmol/I during combined hyperventilation and hypertension. The incremental rise of lactate with combined hyperventilation and hypolension was significant at the end of the second hour of hypotension. Cerebrospinal fluid lactatelpyruvate ratios and CPK increased significantly above control only with combined hyperventilation and hypotension.Oxygen tension of muscle and brain decreased from baseline with hyperventilation alone and decreased further to 2.66 kPa (20 mm Hg) after combined hyperventilation and hypotension. Good correlation was found between changes in oxygen tension of muscle and brain in the three groups (r -0.914, p < 0.05 and r -0.908, p < 0.05), respectively, for all groups combined.Evidence is thus presented that the combination of hyperventilation and hypotension to accepted levels causes inadequate cerebral oxygen supply in anaesthetized dogs. Although muscle and brain oxygen tensions reflected the degree of cerebral hypoxia, their usefulness as clinical monitors is likely to be limited. The work was done in the Department of Anesthesiology, Children's Memorial Hospital, Chicago. It was supported in part by a National Institute of Health Grant, number RR05475-15, and in part by the Northwestern University Department of Anesthesia.Presented at the annual meeting of the American Society of Anesthesiologists, Chicago, Illinois, October, 1978, and the annual meeting of the Anaesthesia Section, The American Academy of Paediatrics, Toronto, Ontario, April, 1979. Reprints requests to: Richard M. Levin, M.D., Department of Anaesthesia, Children's Memorial Hospital, 2300 Children's Plaza, Chicago, Illinois, 60614 U.S.A.Canad. Anaesth. Soc. J., vol. 27, no. 3, May 1980 anaesthetic adjuncts combine cerebral vaso. constriction and decreased cerebral perfusion t( reduce brain size and produce a drier operativ~ field for more precise surgical dissection and re duced blood loss. t'2 Hyperventilati0n anc h...