Cerebral Blood Flow and Metabolic Changes from Induction to Onset of Anesthesia with Halothane or Pentobarbital

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Abstract
The effects of halothane inhalation (2%) and infusion of sodium pentobarbital (1.43 mg/kg/min) on cerebral blood flow (CBF) and metabolic rate (CMRO2) were evaluated in goats from induction to the onset of anesthesia (loss of response to pain) and upon emergence from anesthesia (regaining response to pain). Halothane doubled CBF (79 .+-. 16-152 .+-. 20 ml/100 g/min) within the 1st 4 min of inhalation without causing anesthesia or any significant change in CMRO2. Anesthesia occurred after 7-8 min of inhalation, at which time CMRO2 was decreased by 12 .+-. 3% (mean .+-. SD) of the awake value. After 20 min of inhalation, CMRO2 was further decreased to 32 .+-. 6% of the awake value, whereupon halothane administration was terminated. Emergence from halothane anesthesia occurred while CMRO2 was still decreased 20 .+-. 4%. Pentobarbital infusion produced a progressive decrease in CBF that paralleled the decrease in CMRO2. Anesthesia occurred when CMRO2 was decreased by 31 .+-. 4% and emergence from anesthesia occurred while CMRO2 was still depressed by 21 .+-. 5%. The data indicated that halothane caused cerebral vasodilation in a way unrelated to CMRO2 and that loss of response to pain during halothane or pentobarbital anesthesia occurred independent of changes in CMRO2.

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