疏血通对沙土鼠脑缺血再灌注损伤的保护作用及其对NO、NOS含量的影响

目的　探讨疏血通对沙土鼠脑缺血再灌注损伤的保护作用。方法　 4 8只成年雄性沙土鼠随机分成假手术组、缺血再灌注组和治疗组 ,阻断双侧颈总动脉 7分钟后血液复流 ,制成沙土鼠脑缺血再灌注模型。每组随机取 8只沙土鼠于再灌注后 2 4小时处死 ,分离出海马区及额顶部脑组织 ,作脑组织匀浆。测定脑组织匀浆中的NO、NOS含量 ,同时对再灌注后 12小时、3天、7天海马区的病理学改变进行观察。然后比较假手术组、缺血再灌注组和治疗组上述指标的变化。结果　缺血再灌注后 12小时治疗组较缺血再灌注组海马CA1区神经元变性、坏死程度明显减轻 ,随再灌注时间的推移两组变性、坏死及形态不规则的神经元均逐渐增多 ;超微结构显示治疗组细胞器、细胞核及细胞内膜系统的损伤性改变较缺血再灌注组明显减轻。治疗组NO、NOS含量则明显低于缺血再灌注组 (P <0 .0 5 ) ,而缺血再灌注组NO、NOS含量明显高于假手术组 (P <0 .0 5 ) ;治疗组与假手术组NO、NOS含量差别无显著性 (P >0 .0 5 )。结论　疏血通可能通过抑制NO合成来对脑缺血再灌注损伤发挥保护作用。

Protective effects of Shuxuetong on gerbil cerebral ischemia-reperfusion injury and influnce to NO and NOS

Objective To study the protective effect of Shuxuetong on gerbil brain tissue in the area of ischemia reperfusion.Methods 48 male gerbils were divided into three groups: false operation group, ischemia reperfusion group and treatment group. Cerebral ischemia reperfusion in gerbils was made by transient clipping bilateral common carotid arteries for 7 minute 8 gerbils were selected at random and put to death in 24 hours after reperfusion in each group. Hippocampal and frontal parietal tissues were separated for making hemogeneity Contents of NO and NOS of brain tissue were measured in 24 hours after reperfusion. Pathological changes in the hippocampal tissue were observed at different time (12th hours, 3th days and 7th days after reperfusion). The difference of above indices among false operation group, ischemia reperfusion group and treatment group was compared.Results Degeneration and necrosis of hippocampal neurons significantly relieved in 12 hours after reperfusion in treatment group compared with ischemia reperfusion group. The injuries of organell, cell nucleus and membrane system more relieved in treatment group than in ischemia reperfusion group. The contents of NO and NOS in treatment group significantly decreased compared with ischemia reperfusion group ( P < 0.05 ) but therre was no difference between treatment group and false operation group ( P > 0.05 ) .Conclusions Shuxuetong has protective effect on brain tissue of ischemia reperfusion by inhibiting synthesis of NO.