Berger R, Jensen A, Paschen W
Department of Obstetrics and Gynecology, University of Bochum, Germany.
Neurosci Lett. 1998 Apr 10;245(3):163-6. doi: 10.1016/s0304-3940(98)00211-0.
The aim of this study was to investigate the role of nitric oxide in metabolic disturbances induced in brain tissue of fetal guinea pigs by oxygen-glucose deprivation. Experiments were performed on hippocampal slices so as to exclude the effects of nitric oxide on the cardiovascular system. Metabolic disturbances were assessed by measuring changes in energy metabolism and protein synthesis after different periods of oxygen-glucose deprivation (OGD). Ten min after OGD of 40 min duration, the concentration of cGMP in tissue slices rose from 1.35 +/- 0.38 to 18.6 +/- 1.04 pmol/mg protein (P < 0.05). This rise was almost completely inhibited by the addition of 100 microM N-nitro-L-arginine (NNLA), indicating that NO-synthase was strongly activated after OGD in fetal brain tissue. However, addition of NNLA improved neither protein synthesis nor energy metabolism measured 12 h after OGD. Thus, nitric oxide does not appear to contribute directly to processes leading to metabolic disturbances induced by transient ischemia in immature brain tissue.
本研究的目的是探讨一氧化氮在氧糖剥夺诱导的胎豚鼠脑组织代谢紊乱中的作用。实验在海马切片上进行，以排除一氧化氮对心血管系统的影响。通过测量不同时间段氧糖剥夺（OGD）后能量代谢和蛋白质合成的变化来评估代谢紊乱。在持续40分钟的OGD后10分钟，组织切片中cGMP的浓度从1.35±0.38升高至18.6±1.04 pmol/mg蛋白质（P<0.05）。添加100μM N-硝基-L-精氨酸（NNLA）几乎完全抑制了这种升高，表明OGD后胎脑组织中的一氧化氮合酶被强烈激活。然而，添加NNLA在OGD后12小时测量时，既未改善蛋白质合成也未改善能量代谢。因此，一氧化氮似乎并未直接参与导致未成熟脑组织短暂缺血诱导的代谢紊乱的过程。
