Kamezawa T, Asakura T, Yatsushiro K, Niiro M, Kasamo S, Fujimoto T
Department of Neurosurgery, Kagoshima University School of Medicine, Japan.
Acta Neurochir Suppl (Wien). 1994;60:499-501. doi: 10.1007/978-3-7091-9334-1_136.
The aim of the present study was to determine the effects of a hyperosmotic agent, 10% glycerol, on both brain energy metabolism and intracellular pH (pHi) in experimental vasogenic brain edema. Vasogenic brain edema was induced by cold injury applied to bilateral parietal portions in 13 mongrel dogs (7 glycerol, 6 control) while, 3 dogs were used as control. Before and at 24 hours after the injury, sequential phosphorous-31 magnetic resonance spectroscopy (31P-MRS) was performed for 2 hours in order to determine phosphocreatine (PCr), beta-adenosine triphosphate (beta-ATP), inorganic phosphate (Pi) levels and pHi. At 24 hours following cold injury, both PCr/Pi and ATP/Pi ratios significantly decreased from 7.75 to 3.97 and from 2.26 to 1.25, respectively. Furthermore, a moderate decrease in pHi of 7.16 to 7.01 was significantly demonstrated during the same experimental period. Administration of glycerol for 30 minutes significantly increased PCr/Pi from 3.97 to 5.06 and ATP/Pi from 1.25 to 1.72, respectively. Also, glycerol administration caused a significant increase in pHi from 7.01 to 7.11. This study indicates that cryogenic injury, in which formation and expansion of vasogenic brain edema a known to occur, results in disturbed brain energy metabolism and in intracellular acidosis; moreover, the administration of glycerol can ameliorate either or both of these derangements.
本研究的目的是确定高渗剂10%甘油对实验性血管源性脑水肿时脑能量代谢和细胞内pH值(pHi)的影响。对13只杂种犬(7只甘油组,6只对照组)双侧顶叶进行冷损伤诱导血管源性脑水肿,另3只犬作为正常对照。在损伤前及损伤后24小时,连续进行2小时的磷-31磁共振波谱(31P-MRS)检查,以测定磷酸肌酸(PCr)、β-三磷酸腺苷(β-ATP)、无机磷酸(Pi)水平及pHi。冷损伤后24小时,PCr/Pi和ATP/Pi比值分别从7.75显著降至3.97,从2.26显著降至1.25。此外,在同一实验期间,pHi从中度下降,从7.16降至7.01。给予甘油30分钟后,PCr/Pi分别从3.97显著升至5.06,ATP/Pi从1.25显著升至1.72。同时,甘油给药使pHi从7.01显著升至7.11。本研究表明,已知会发生血管源性脑水肿形成和扩张的低温损伤会导致脑能量代谢紊乱和细胞内酸中毒;此外,给予甘油可改善这些紊乱中的一种或两种情况。