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The effects of inhalation of halothane (2 per cent) 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 to l52 ± 20 ml/100g/min) within the first 4 minutes of inhalation without causing anesthesia or any significant change in CMRO2. Anesthesia occurred after 7–8 minutes of inhalation, at which time CMRO2 was decreased by 12 ± 3 per cent (mean ± SD) of the awake value. After 20 minutes of inhalation, CMRO2 was further decreased to 32 ± 6 per cent of the awake value, whereupon halothane administration was terminated. Emergence from halothane anesthesia occurred while CMRO2 was still decreased 20 ± 4 per cent. Pentobarbital infusion produced a progressive decrease in CBF that paralleled the decrease in CMRO2. Anesthesia occurred when CMRO2 was decreased by 31 ± 4 per cent and emergence from anesthesia occurred while CMRO2 was still depressed by 21 ± 5 per cent. The data from this study indicate that halothane causes cerebral vasodilation in a way unrelated to CMRO2 and that loss of response to pain during halothane or pentobarbital anesthesia occurs independent of changes in CMRO2.
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Albrecht et al. (1977) studied this question.
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