摘要
目的探讨Na+-K+-ATP酶活性与缺血半暗带(IP)脑组织再灌注损伤的关系。方法 75只雄性Wistar大鼠随机分为假手术组15只,模型组60只。模型组又根据缺血再灌注时间分为6、24、48及72h4个时间点,每个时间点15只。模型组采用线栓法制备缺血2h再灌注模型。2组大鼠分别于再灌注6、24、48、72h断头取脑,观察IP脑组织Na+-K+-ATP酶活性、神经症状评分、脑组织水肿程度及脑梗死范围的变化。结果与假手术组比较,模型组大鼠IP脑组织Na+-K+-ATP酶活性明显降低(P<0.05),大鼠神经症状评分、脑组织含水量及脑梗死面积明显升高(P<0.05)。随着缺血再灌注时间的延长,大鼠神经症状评分、脑组织含水量均在48h升至最高,IP脑组织Na+-K+-ATP酶活性在48h降至最低,脑梗死面积在72h达最大值。结论在IP脑组织缺血再灌注损伤过程中,Na+-K+-ATP酶活性的改变起着至关重要的作用。
Objective To study the relation between Na^＋-K^＋-ATPase activities and I/R injury in ischemic penumbra tissue. Methods Seventy-five male Wistar rats were randomly divided into sham operation group（n=15） and model group（n=60）. The model group was further divided into 6,24,48 and 72 h I/R groups（15 in each group）. An I/R model was established with thread method. Brain tissue was taken out from the rats at 6,24,48 and 72 h after reperfusion. The Na^＋-K^＋-ATPase activities, neurological symptoms, brain edema and cerebral infarction size were observed. Results The Na^＋-K^＋-ATPase activities, neurological symptom scores, brain water content and cerebral infarction size were significantly higher in model group than in sham operation group （P〈0.05）. The neurological symptom scores and brain water content reached their peak at 48 h, the Na^＋-K^＋-ATPase activities reached their minimum at 48 h,the cerebral infarction size reached its peak at 72 h after I/R injury. Conclusion The Na^＋-K^＋-ATPase activities play a vital role in rat penumbra tissue I/R injury.
出处
《中华老年心脑血管病杂志》
CAS
北大核心
2013年第3期302-304,共3页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基金
广西自然科学基金(0991212)
关键词
钠钾交换ATP酶
脑缺血
再灌注损伤
神经元
细胞凋亡
sodium-potassium-exchanging ATPase
brain ischemia
reperfusion injury
neurons
apoptosis
