T. Fujibayashi et al., BRAIN ENERGY-METABOLISM AND BLOOD-FLOW DURING SEVOFLURANE AND HALOTHANE ANESTHESIA - EFFECTS OF HYPOCAPNIA AND BLOOD-PRESSURE FLUCTUATIONS, Acta anaesthesiologica Scandinavica, 37(8), 1993, pp. 806-810
The effects of halothane and sevoflurane on cat brain energy metabolis
m and regional cerebral blood flow (rCBF) were evaluated during normo-
and hypocapnia. Brain energy status was evaluated with phosphorous nu
clear magnetic resonance spectroscopy (P-31-MRS) and rCBF was measured
by the hydrogen clearance method. A high concentration of halothane (
3 MAC) impaired brain energy metabolism, while even a higher concentra
tion of sevoflurane (4 MAC) had no untoward effect on brain energy met
abolism. At 3 MAC of halothane, there were measurable decreases in bra
in phosphocreatine (69% of the control) and increases in brain inorgan
ic phosphate (about 250% of control Pi), even though CBF was about 70%
of the control value. During hypocapnia, the phosphocreatine levels b
egan to decrease at a PaCO2 of 2.7 kPa with 2 MAC of sevoflurane (90%
of the control), and at a PaCO2 of 4.0 kPa with 2 MAC of halothane (92
% of the control). rCBF had decreased to less than 50% of the control
value when Paco2 was less-than-or-equal-to 2.7 kPa with 2 MAC of sevof
lurane and less-than-or-equal-to 4.0 kPa with 2 MAC of halothane. Abno
rmal brian energy metabolism was only observed when rCBF was decreased
to less than half of the control (non-anesthetized and normocapnic) v
alue. Following administration of a vasopressor, metaraminol, the abno
rmal brain energy metabolism induced by 2 MAC of halothane at a PaCO2
of 1.33 kPa was normalized in parallel with the improved rCBF values.
We conclude that hyperventilation and fluctuating blood pressure contr
ibute to the occurrence of abnormal brain energy metabolism during hal
othane and sevofluranc anesthesia. This is more pronounced with haloth
ane than with sevoflurane. The hypocapnia-induced abnormality during e
xposure to 2 MAC of either agent was due to decreased CBF associated w
ith low perfusion pressure, indicating that there was no direct effect
of these anesthetics on cerebral energy metabolism.