Röhn G, Schlenker M, Paschen W
Max-Planck Institute for Neurological Research, Department of Experimental Neurology, Cologne, Germany.
Exp Neurol. 1992 Aug;117(2):210-5. doi: 10.1016/0014-4886(92)90129-e.
Mongolian gerbils were anesthetized with halothane and forebrain ischemia was induced by occluding both common carotid arteries. After 2, 4, 6, 8, or 10 min of vascular occlusion clips were removed and animals allowed to recover for 8 or 24 h. At the end of the experiments animals were reanesthetized and their brains frozen in situ. Tissue samples were taken from the cerebral cortex, striatum, hippocampus, and thalamus for determination of ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAMDC) activity by measurement of the release of 14CO2 from [14C]ornithine and S-[14C]adenosylmethionine, respectively. A transient increase in ODC activity was found after 8 h of recirculation following cerebral ischemia in all brain structures studied. ODC activity was significantly increased after 8 h of recirculation in the hippocampus of animals subjected to 4 min of ischemia, in the cortex and striatum after 6 min of ischemia, and in the thalamus after 8 min of vascular occlusion. ODC activity had already reached a plateau in the hippocampus after 4 min of vascular occlusion and in the cortex, striatum, and thalamus after 8 min, since there is no further increase in activity even after 10 min of ischemia. After cerebral ischemia and 24 h of recirculation ODC activity returned to control levels throughout the forebrain regardless of the duration of ischemia. SAMDC activity was significantly reduced after 8 h of recirculation following 4 to 10 min of ischemia in the cortex and 8 min of ischemia in the striatum.(ABSTRACT TRUNCATED AT 250 WORDS)
蒙古沙鼠用氟烷麻醉,通过阻断双侧颈总动脉诱导前脑缺血。在血管阻断2、4、6、8或10分钟后,移除夹子,让动物恢复8或24小时。实验结束时,动物再次麻醉,其大脑原位冷冻。从大脑皮层、纹状体、海马体和丘脑采集组织样本,分别通过测量[14C]鸟氨酸和S-[14C]腺苷甲硫氨酸释放的14CO2来测定鸟氨酸脱羧酶(ODC)和S-腺苷甲硫氨酸脱羧酶(SAMDC)活性。在所研究的所有脑结构中,脑缺血后再灌注8小时后发现ODC活性短暂增加。在缺血4分钟的动物海马体中,再灌注8小时后ODC活性显著增加;缺血6分钟后,皮层和纹状体中ODC活性显著增加;血管阻断8分钟后,丘脑中ODC活性显著增加。血管阻断4分钟后,海马体以及8分钟后皮层、纹状体和丘脑中的ODC活性已达到平台期,因为即使缺血10分钟后活性也没有进一步增加。脑缺血和再灌注24小时后,无论缺血持续时间如何,整个前脑的ODC活性都恢复到对照水平。在皮层缺血4至10分钟以及纹状体缺血8分钟后再灌注8小时,SAMDC活性显著降低。(摘要截断于250字)