Fujibayashi T, Sugiura Y, Yanagimoto M, Harada J, Goto Y
Department of Anesthesiology, Fukui Medical School, Japan.
Acta Anaesthesiol Scand. 1993 Nov;37(8):806-10. doi: 10.1111/j.1399-6576.1993.tb03813.x.
The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood flow (rCBF) were evaluated during normo- and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy (31P-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 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 < or = 2.7 kPa with 2 MAC of sevoflurane and < or = 4.0 kPa with 2 MAC of halothane. Abnormal brain energy metabolism was only observed when rCBF was decreased to less than half of the control (non-anesthetized and normocapnic) value. Following administration of a vasopressor, metaraminol, the abnormal 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 contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)
在正常碳酸血症和低碳酸血症期间，评估了氟烷和七氟醚对猫脑能量代谢及局部脑血流（rCBF）的影响。采用磷核磁共振波谱法（31P-MRS）评估脑能量状态，通过氢清除法测量rCBF。高浓度氟烷（3MAC）损害脑能量代谢，而更高浓度的七氟醚（4MAC）对脑能量代谢无不良影响。在3MAC氟烷时，尽管脑血流约为对照值的70%，但脑磷酸肌酸有可测量的降低（为对照值的69%），脑无机磷酸盐增加（约为对照无机磷酸盐的250%）。在低碳酸血症期间，使用2MAC七氟醚时，当动脉血二氧化碳分压（PaCO2）为2.7kPa时磷酸肌酸水平开始降低（为对照值的90%），使用2MAC氟烷时，当PaCO2为4.0kPa时磷酸肌酸水平开始降低（为对照值的92%）。当使用2MAC七氟醚且PaCO2≤2.7kPa以及使用2MAC氟烷且PaCO2≤4.0kPa时，rCBF降至对照值的50%以下。仅当rCBF降至对照（未麻醉且正常碳酸血症）值的一半以下时才观察到异常脑能量代谢。给予血管升压药间羟胺后，在PaCO2为1.33kPa时由2MAC氟烷诱导的异常脑能量代谢与改善的rCBF值同时恢复正常。我们得出结论，过度通气和血压波动促成了氟烷和七氟醚麻醉期间异常脑能量代谢的发生。氟烷比七氟醚更明显。（摘要截短于250字）
