Horváth E, Warmuth I, Zilles Z, Traber J
Institute for Neurobiology, Troponwerke, Köln, FRG.
Stroke. 1990 Dec;21(12 Suppl):IV126-9.
The quantitative [14C]-2-deoxy-D-glucose autoradiographic method was used to compare the acute effects of the Ca2+ channel antagonist nimodipine (10 mg/kg) and the Ca2+ channel activator Bay K 8644 (1.25 mg/kg) on local cerebral glucose utilization of rat brain after single, intraperitoneal application. Nimodipine reduced glucose metabolism significantly in 23 of the 49 brain regions evaluated. Bay K 8644 decreased the local cerebral glucose utilization to an even greater extent in all regions studied. The anatomic localization of those regions with the largest decrease of glucose utilization was almost identical for both drugs (globus pallidus, hippocampus, geniculate body, substantia nigra, and entorhinal cortex). No increase in glucose metabolism was measured in any of the brain areas evaluated.
采用定量[14C]-2-脱氧-D-葡萄糖放射自显影法，比较腹腔注射一次Ca2+通道拮抗剂尼莫地平（10mg/kg）和Ca2+通道激动剂Bay K 8644（1.25mg/kg）后对大鼠脑局部葡萄糖利用的急性影响。在所评估的49个脑区中，尼莫地平使23个脑区的葡萄糖代谢显著降低。Bay K 8644在所有研究区域均使局部脑葡萄糖利用降低得更为明显。两种药物使葡萄糖利用降低幅度最大的那些区域的解剖定位几乎相同（苍白球、海马、膝状体、黑质和内嗅皮质）。在所评估的任何脑区均未检测到葡萄糖代谢增加。
