BRAIN ENERGY-METABOLISM AND BLOOD-FLOW DURING SEVOFLURANE AND HALOTHANE ANESTHESIA - EFFECTS OF HYPOCAPNIA AND BLOOD-PRESSURE FLUCTUATIONS (VOL 37, PG 806, 1993)

Citation
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
Citations number
23
Categorie Soggetti
Anesthesiology
ISSN journal
00015172
Volume
38
Issue
4
Year of publication
1994
Pages
413 - 418
Database
ISI
SICI code
0001-5172(1994)38:4<413:BEABDS>2.0.ZU;2-9
Abstract
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.