BRAIN ENERGY-METABOLISM AND BLOOD-FLOW DURING SEVOFLURANE AND HALOTHANE ANESTHESIA - EFFECTS OF HYPOCAPNIA AND BLOOD-PRESSURE FLUCTUATIONS (VOL 37, PG 806, 1993)
T. Fujibayashi et al., BRAIN ENERGY-METABOLISM AND BLOOD-FLOW DURING SEVOFLURANE AND HALOTHANE ANESTHESIA - EFFECTS OF HYPOCAPNIA AND BLOOD-PRESSURE FLUCTUATIONS (VOL 37, PG 806, 1993), Acta anaesthesiologica Scandinavica, 38(4), 1994, pp. 413-418
The effects of halothane and sevoflurane on cat brain energy metabolis
m and regional cerebral blood now (rCBF) were evaluated during normo-
and hypocapnia. Brain energy status was evaluated with phosphorous nuc
lear 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 concentrat
ion of sevoflurane (4 MAC) had no untoward effect on brain energy meta
bolism. At 3 MAC of halothane, there were measurable decreases in brai
n phosphocreatine (69% of the control) and increases in brain inorgani
c phosphate (about 250% of control Pi), even though CBF was about 70%
of the control value. During hypocapnia, the phosphocreatine levels be
gan to decrease at a Paco(2) of 2.7 kPa with 2 MAC of sevoflurane (90%
of the control), and at a Paco(2) of 4.0 kPa with 2 MAC of halothane
(92% of the control). rCBF had decreased to less than 50% of the contr
ol value when Paco(2) was less than or equal to 2.7 kPa with 2 MAC of
sevoflurane and less than or equal to 4.0 kPa with 2 MAC of halothane.
Abnormal brain energy metabolism was only observed when rCBF was decr
eased to less than half of the control (non-anesthetized and normocapn
ic) value. Following administration of a vasopressor, metaraminol, the
abnormal brain energy metabolism induced by 2 MAC of halothane at a P
aco(2) of 1.33 kPa was normalized in parallel with the improved rCBF v
alues. We conclude that hyperventilation and fluctuating blood pressur
e contribute to the occurrence of abnormal brain energy metabolism dur
ing halothane and sevoflurane anesthesia. This is more pronounced with
halothane than with sevoflurane. The hypocapnia-induced abnormality d
uring exposure to 2 MAC of either agent was due to decreased CBF assoc
iated with low perfusion pressure, indicating that there was no direct
effect of these anesthetics on cerebral energy metabolism.