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目的 :观察丙戊酸钠对沙土鼠单侧脑缺血再灌注的保护作用。方法 :4 0只雄性蒙古沙土鼠随机分为 2组。左颈内动脉钳夹 30min后使血流再通 ,缺血开始后即以微量灌注泵自颈外静脉分别注入丙戊酸钠 60mg·kg- 1(治疗组 )和 0 .9%氯化钠注射液 (对照组 ) ,流速 0 .5mL·h- 1,历时 2h。术后15h ,每组随机取 10只测血浆神经元特异性烯醇化酶 (NSE) ,术后 7d ,2组脑组织冠状切片以免疫组织化学染色观察海马神经元形态。结果 :治疗组神经缺损记分 1.5分± 0 .6分 ,对照组 3.2分± 0 .8分 ;治疗组血浆NSE含量 64μg± 12 μg ,对照组 12 8μg± 2 0 μg ;海马神经元损害程度治疗组 1.4分±0 .8分 ,对照组 2 .9分± 0 .8分。t检验均有显著差异 (P <0 .0 5)。结论 :静注丙戊酸钠对沙土鼠脑缺血再灌注有保护作用。
Objective: To observe the protective effect of sodium valproate on unilateral cerebral ischemia-reperfusion in gerbils. Methods: 40 Mongolian gerbils were randomly divided into two groups. After 30 minutes of left internal carotid artery clamp, the blood flow was recanalized. After the onset of ischemia, micro-perfusion pump was used to inject 60 mg · kg -1 valproate (treatment group) and 0.9% sodium chloride Injection (control group), the flow rate of 0.5mL · h-1, lasted 2h. At 15h after operation, 10 rats in each group were randomly divided into three groups. Neuronal specific enolase (NSE) was measured in each group. The morphology of hippocampal neurons was observed by immunohistochemical staining on the 7th day after operation. Results: The score of neurological deficit in the treatment group was 1.5 ± 0.6, the control group was 3.2 ± 0. 8; the plasma NSE level in the treatment group was 64 μg ± 12 μg, and the control group was 12 8 μg ± 20 μg; the degree of damage in the hippocampal neurons was Group 1.4 points ± 0.8 points, control group 2.9 points ± 0.8 points. t test were significantly different (P <0. 05). Conclusion: Sodium valproate has a protective effect on gerbil cerebral ischemia and reperfusion.