INVESTIGATION OF MOLECULAR MECHANISM ON ISCHEMIC

1)对脑能量代谢的影响用成年大鼠进行的实验研究表明，单次扩散性抑制(SD)负荷可引起直接刺激的皮质局部酸中毒，继而波及同侧全脑。这一变化在刺激20分钟后恢复。ATP组织化学显示与组织pH变化相同的变化。重复负荷120min引起酸中毒和ATP耗竭-45min，刺激60min后恢复。2)SD预负荷可抑制脑缺血诱导的大脑皮层细胞凋亡，但不抑制大脑皮层的坏死。3)对钙稳态的影响SD负载后未见钙离子的组织化学改变。因此，本研究表明SD对脑缺血诱导的大脑皮层细胞凋亡有保护作用。

1)Effect on brain energy metabolismExperimantal study using adult rats revealed that loading of single spreading depression (SD) cause local acidosis in the cortex stimulated directly., followed by it extension into the ipsilateral whole hemisphere. This change was recooverd 20 minutes after stimulation. ATP histochemistry showed same change as that of tissue pH change. The repetitive loading for 120 minutes caused acidosis and ATP depletion for- 45 minutes, which was recovered 60 minutes after stimulation. Thereafter, no change could induced up to six hours later.2)Effect on apoptosisApotosis in the cerebral cortex induced by cerebral ischemia was suppressed by preloading of SD.In contrast, necrosis in the cerebral corrtex was not suppredded.3)Effect on calcium homeostasisNo calcium ion change was observed histochemically on SD loading.Thus, present study revealed that SD protected apoptotic cell death in the cerebral cortex induced by cerebral ischemia.