Kass I S, Amorim P, Chambers G, Austin D, Cottrell J E
Department of Anesthesiology, State University of New York Health Science Center at Brooklyn 11203, USA.
J Neurosurg Anesthesiol. 1997 Jul;9(3):280-6. doi: 10.1097/00008506-199707000-00015.
It is unclear whether isoflurane protects against neuronal damage. This study examines the extent and mechanism by which isoflurane might affect anoxic neuronal damage. The size of the evoked postsynaptic population spike recorded from the CA 1 pyramidal cell layer of the rat hippocampal slice 60 min after anoxia was compared with its preanoxic, preisoflurane level. Intracellular adenosine triphosphate (ATP), sodium, and potassium levels were measured in the dentate and CA 1 regions at the end of the anoxic period in similarly treated slices. Isoflurane increased the latency and reduced the amplitude of the evoked response before anoxia. Isoflurane (2%) did not significantly improve recovery of the evoked response after 5 min of anoxia (untreated slices = 6 +/- 2% (mean +/- SEM), isoflurane = 17 +/- 7%); 1.5% isoflurane also did not significantly improve recovery after 4 min of anoxia (untreated = 30 +/- 8% vs. 1.5% isoflurane = 47 +/- 12%). Isoflurane did not significantly attenuate the decrease in ATP levels in either the dentate or CA 1 regions of the hippocampal slice during 4 or 7 min of anoxia; however, there was a significant improvement in ATP levels after 10 min of anoxia in both regions of isoflurane-treated preparations (1.0 +/- 0.1 vs. 1.4 +/- 0.1, CA 1; 1.3 +/- 0.1 vs. 2.0 +/- 0.2 nM/mg dry weight, dentate). Sodium concentrations increased and potassium concentrations decreased during anoxia. Isoflurane did not significantly attenuate the changes in these ions during anoxia. In conclusion, isoflurane does not significantly improve recovery of CA 1 pyramidal cells during anoxia nor does it attenuate the anoxic changes in ATP, sodium, and potassium after 4 or 7 min of anoxia. With a more prolonged period of anoxia (10 min) isoflurane reduces the decrease in ATP levels.
异氟烷是否能预防神经元损伤尚不清楚。本研究探讨了异氟烷可能影响缺氧性神经元损伤的程度及机制。将缺氧60分钟后从大鼠海马切片CA1锥体细胞层记录的诱发突触后群体峰电位大小与其缺氧前、异氟烷处理前的水平进行比较。在类似处理的切片缺氧期结束时，测量齿状回和CA1区的细胞内三磷酸腺苷（ATP）、钠和钾水平。异氟烷增加了缺氧前诱发反应的潜伏期并降低了其幅度。异氟烷（2%）在缺氧5分钟后并未显著改善诱发反应的恢复情况（未处理切片 = 6±2%（平均值±标准误），异氟烷 = 17±7%）；1.5%异氟烷在缺氧4分钟后也未显著改善恢复情况（未处理 = 30±8% 对比 1.5%异氟烷 = 47±12%）。在缺氧4分钟或7分钟期间，异氟烷并未显著减轻海马切片齿状回或CA1区ATP水平的下降；然而，在异氟烷处理的制剂中，缺氧10分钟后两个区域的ATP水平均有显著改善（CA1区：1.0±0.1对比1.4±0.1；齿状回：1.3±0.1对比2.0±0.2 nM/毫克干重）。缺氧期间钠浓度升高而钾浓度降低。异氟烷在缺氧期间并未显著减轻这些离子的变化。总之，异氟烷在缺氧期间并未显著改善CA1锥体细胞的恢复情况，在缺氧4分钟或7分钟后也未减轻ATP、钠和钾的缺氧变化。在更长时间的缺氧（10分钟）情况下，异氟烷可减少ATP水平的下降。
