巴曲酶对沙土鼠脑缺血再灌注损伤的影响

研究巴曲酶对脑缺血再灌注所致延迟性神经元死亡的影响以及与ＯＨ·产生的关系． 沙土鼠前脑缺血１０ ｍ ｉｎ 再灌注６０ ｍ ｉｎ． 应用高效液相色谱法测定纹状体多巴胺，海马ＡＴＰ和２，３－二羟基苯甲酸（２，３－ＤＨＢＡ， 反映ＯＨ·含量）的含量． 应用病理方法检查海马ＣＡ１ 区锥体细胞延迟性死亡情况．结果显示， 在再灌注开始时ｉｐ 巴曲酶８ ＢＵ·ｋｇ－ １明显促进海马ＡＴＰ含量的恢复，减少ＯＨ·的产生和纹状体多巴胺的释放． 脑缺血再灌注后ｄ ７ 巴曲酶组（８ ＢＵ·ｋｇ－ １ ｉｐ，每日１ 次，共３ ｄ）海马ＣＡ１ 区存活的锥体细胞数目也明显多于对照组（每１００ 平方微米０．２７±０．１１ ｖｓ ０．０４±０．０３）． 以上结果提示， 巴曲酶可减轻脑缺血再灌注所致的延迟性神经元死亡， 其机理可能与其减少脑缺血再灌注期间ＯＨ·的产生有关．

Effect of batroxobin on cerebral ischemia/reperfusion injury in gerbils

To study the effect of batroxobin(Bat) on delayed neuron death (DND) and the involvement of hydroxyl radical(OH·) production during cerebral ischemia/reperfusion in DND. Gerbils were subjected to 10 min of forebrain ischemia followed by 60 min of reperfusion. The contents of dopamine (DA) in striatum and ATP, 2,3-dihydroxybenzoic (2,3-DHBA) in hippocampus were determined by high- performance liquid chromatography. The DND was assessed by histological examination. The results showed that ip Bat 8 BU·kg^-1 at the initiation of reperfusion obviously enhanced the recovery of ATP content and decreased the content of 2,3-DHBA in hippocampus and DA release in striatum. There were more surviving neurons in hippocampal CA1 sector in Bat group (8 BU·kg^-1 ip, once a day for 3 d) than in ischemia/reperfusion group (0.27±0.11 vs 0.04±0.03 per 100 square micron) 7 d later. The results suggest that Bat reduces the cerebral ischemia/reperfusion injury-induced DND, and the mechanism is related to its role of decreasing the OH· generation during cerebral ischemia/reperfusion.