摘要
目的探讨大鼠局灶性脑缺血时脑微血管、脑组织中一氧化氮合酶(NOS)的活性变化及其与脑损伤的关系。方法将Wistar雄性大鼠73只随机分为假手术组19只;缺血组54只,据缺血时间1、2、3、4h再分Ⅰ1、Ⅰ2、Ⅰ3、Ⅰ4组。用线栓法制备大鼠大脑中动脉闭塞模型,用放射性同位素法测定脑微血管及脑组织中NOS的活性。结果局灶性脑缺血时不同部位、时间,NOS活性的变化不同。脑微血管中NOS活性在缺血4h(Ⅰ4)组为(0.104±0.035)pmol/mg蛋白,假手术组为(0.042±0.021)pmol/mg蛋白,两组比较差异有显著意义(P<0.001)。纹状体、海马的NOS活性在Ⅰ4组分别为(0.037±0.007)pmol/mg蛋白、(0.050±0.010)pmol/mg蛋白,假手术组为(0.079±0.018)pmol/mg蛋白、(0.059±0.008)pmol/mg蛋白,两组比较差异有显著意义(P<0.001,P<0.05)。结论脑微血管中NOS活性变化在局灶性脑缺血损伤中起重要作用,脑组织中NOS活性变化也参与了其病理生理过程。
Objective To investigate the changes of NOS activity in the cerebral mierovessels and cerebral tissues of rat model during focal cerebral ischemia, and its correlation with the cerebral injury. Methods The model was made by blocking the MCAO with thread. The NOS activity of different regions and phases were tested by radioisotopie method. Infarct volume was measured by 2,3,5-triphenyhetrazolium chloride staining and image analysis. Pathological changes were observed mieroscopieally with HE stained sections. Results The NOS activity in the cerebral microvessels after 4 hours ischemia （ 14 was （0. 104 ± 0. 035 ） pmol/mg, protein, obviously higher than that of sham group （0. 042 ± 0. 021 pmol/mg, protein, P 〈 0. 001 ; The NOS aetivity in the striatum and hippocampus was （0. 037 ±0. 007 ） （0. 050 ± 0. 010） pmol/mg, protein respectively, decreased than that of sham group （0. 079 ± 0. 018 ）, （0.059 ±0. 008） pmol/mg, protein （ P 〈 0. 001 , P 〈 0. 05 ）. When infarct vohune enlarged, the remarkable changes of pathology were found. Conclusion NOS activity in the cerebral microvessels is thought to play an important role during the cerebral injury of focal cerebral ischemia, and that in the cerebral tissues may contribute some role too.
出处
《中国脑血管病杂志》
CAS
2005年第9期407-410,共4页
Chinese Journal of Cerebrovascular Diseases
关键词
脑缺血
一氧化氮合酶
脑微血管
脑组织
Brain ischemia
Nitria oxide synthase
Cerebral microvessels
Cerebral tissues
