Xie Y, Seo K, Hossmann K A
Max-Planck-Institut für neurologische Forschung, Abteilung für experimentelle Neurologie, Köln, F.R.G.
J Neurol Sci. 1989 Sep;92(2-3):317-28. doi: 10.1016/0022-510x(89)90146-9.
The effect of barbiturate treatment on post-ischemic cerebral protein biosynthesis was studied in gerbils subjected to 5 min transient occlusion of carotid arteries followed by 2 h or 48 h recirculation. Ischemia induced a remarkable decline of amino acid incorporation into brain proteins in most forebrain structures. The initial inhibition recovered to near normal after 2 days recirculation in all regions except the vulnerable CA1 sector. Barbiturate treatment, which previously has been shown to prevent delayed neuronal death in CA1 sector, did not ameliorate the initial inhibition of protein synthesis but it significantly improved subsequent recovery, especially in the vulnerable CA1 sector of hippocampus. These observations indicate that delayed neuronal death in CA1 sector of hippocampus results from selective failure of post-ischemic recovery and not from selective ischemic injury of the protein synthesizing machinery. This explains that delayed neuronal death can be prevented by therapeutic interventions which are initiated during the post-ischemic recirculation phase.
在沙土鼠中研究了巴比妥酸盐治疗对缺血后脑蛋白生物合成的影响，这些沙土鼠经历了5分钟的颈动脉短暂闭塞，随后再灌注2小时或48小时。缺血导致大多数前脑结构中氨基酸掺入脑蛋白的显著下降。除了易损的CA1区外，在所有区域再灌注2天后，最初的抑制作用恢复到接近正常水平。先前已证明巴比妥酸盐治疗可预防CA1区延迟性神经元死亡，它并没有改善蛋白质合成的初始抑制，但显著改善了随后的恢复，尤其是在海马体易损的CA1区。这些观察结果表明，海马体CA1区延迟性神经元死亡是由于缺血后恢复的选择性失败，而不是由于蛋白质合成机制的选择性缺血损伤。这解释了延迟性神经元死亡可以通过在缺血后再灌注阶段开始的治疗干预来预防。
