Lien Y H, Michaelis T, Moats R A, Ross B D
Department of Medicine, University of Arizona, Tucson 85724.
Life Sci. 1994;54(20):1507-12. doi: 10.1016/0024-3205(94)90018-3.
Cerebral myo-inositol depletion is found in patients with hepatic encephalopathy and can be implicated in the pathogenesis of hepatic encephalopathy. We measured scyllo-inositol, a stereoisomer of myo-inositol, in brain extracts from patients dying in hepatic coma using HPLC and high resolution 1H MRS. The cerebral scyllo-inositol concentration, determined by both methods, in patients without hepatic encephalopathy was 0.41 +/- 0.11 mmol/kg wet weight. It decreased by 73% and 76%, respectively, as measured by HPLC and 1H MRS, in patients with hepatic encephalopathy. These findings indicate that myo-inositol depletion in patients with hepatic encephalopathy is not due to enhanced conversion of myo-inositol to scyllo-inositol or inhibition of myo-inositol transport by scyllo-inositol, but rather to the reduced biosynthesis or transport of both inositols.
肝性脑病患者存在脑内肌醇耗竭现象，这可能与肝性脑病的发病机制有关。我们使用高效液相色谱法（HPLC）和高分辨率氢磁共振波谱（1H MRS），测定了死于肝昏迷患者脑提取物中的异肌醇（肌醇的一种立体异构体）。通过这两种方法测定，无肝性脑病患者的脑内异肌醇浓度为0.41±0.11 mmol/kg湿重。在肝性脑病患者中，通过HPLC和1H MRS测定，该浓度分别下降了73%和76%。这些发现表明，肝性脑病患者的肌醇耗竭并非由于肌醇向异肌醇的转化增强，或异肌醇对肌醇转运的抑制，而是由于两种肌醇的生物合成或转运减少。
