Qi L, Dong W
Jilin Air Force Hospital PLA.
Zhonghua Yi Xue Za Zhi. 1992 Jul;72(7):420-3, 447.
In order to study and modify the ischemic brain lesions, protecting the reversible damage of neurons, and limiting the ischemic damage both models of cerebral ischemia--focal cerebral ischemia induced by photochemically, and brain reperfusion after ligation of common carotid arteries bilateral in Wistar rats were used to investigate the protective effect of diphenylhydantoin (DPH) on cerebral ischemia. Two groups of rats received DPH 10 mg/kg and 30 mg/kg respectively were compared with those having received normal saline immediately after cerebral ischemia. The effects of DPH on the changes of EEG, biochemical marker and pathologic lesion in focal cerebral ischemia in rats were evaluated. The results showed that the degree of restoration of EEG in the group treated with DPH was better than in the group with normal saline, the content of water in ischemic cerebral tissue was decreased significantly (P < 0.05), the activity of Na-K-ATPase and antioxidant was increased significantly (P < 0.01, P < 0.05, respectively), and the percentage of necrotic neurons in periischemic area was decreased markedly (P < 0.001) in groups treated by DPH. The results suggest that there is a definite protective effect of DPH on cerebral ischemia.
为了研究和改善缺血性脑损伤,保护神经元的可逆性损伤并限制缺血性损伤,采用两种脑缺血模型——Wistar大鼠光化学诱导的局灶性脑缺血以及双侧颈总动脉结扎后的脑再灌注,来研究苯妥英(DPH)对脑缺血的保护作用。将分别接受10mg/kg和30mg/kg DPH的两组大鼠与脑缺血后立即接受生理盐水的大鼠进行比较。评估了DPH对大鼠局灶性脑缺血脑电图变化、生化标志物及病理损伤的影响。结果显示,DPH治疗组脑电图恢复程度优于生理盐水组,缺血脑组织含水量显著降低(P<0.05),钠钾ATP酶活性及抗氧化能力显著增强(分别为P<0.01、P<0.05),且DPH治疗组缺血周边区坏死神经元百分比显著降低(P<0.001)。结果表明,DPH对脑缺血有确切的保护作用。