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Brain energy metabolism and blood flow during sevoflurane and halo thane anesthesia: effects of hypocapnia and blood pressure fluctuations
Author(s) -
Fujibayashi T.,
Sugiura Y.,
Yanagimoto M.,
Harada J.,
Goto Y.
Publication year - 1993
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1993.tb03813.x
Subject(s) - halothane , phosphocreatine , hypocapnia , cerebral blood flow , medicine , anesthesia , sevoflurane , hyperventilation , endocrinology , energy metabolism , hypercapnia , acidosis
The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood How (rCBF) were evaluated during normo‐ and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy ( 31 P‐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 concentration of sevoflurane (4 MAC) had no untoward effect on brain energy metabolism. At 3 MAC of halothane, there were measurable decreases in brain phosphocreatine (69% of the control) and increases in brain inorganic phosphate (about 250% of control Pi), even though CBF was about 70% of the control value. During hypocapnia, the phosphocreatine levels began 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 control value when Paco 2 was ≤2.7 kPa with 2 MAC of sevoflurane and ≤4.0 kPa with 2 MAC of halothane. Abnormal brian energy metabolism was only observed when rCBF was decreased to less than half of the control (non‐anesthetized and normocapnie) value. Following administration of a vasopressor, metaraminol, the abnormal brain energy metabolism induced by 2 MAC of halothane at a Paco 2 of 1.33 kPa was normalized in parallel with the improved rCBF values. We conclude that hyperventilation and fluctuating blood pressure contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane. The hypocapnia‐induced abnormality during exposure to 2 MAC of either agent was due to decreased CBF associated with low perfusion pressure, indicating that there was no direct effect of these anesthetics on cerebral energy metabolism.