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目的观察重度局灶性脑缺血大鼠尾壳核一氧化氮合酶(NOS)表达过程,为脑缺血的发病机理研究提供解剖形态学依据。方法SD大鼠40只,随机分为5组:(1)正常对照组;(2)假手术组;(3)脑缺血1 h组;(4)脑缺血6 h组;(5)脑缺血24 h组。每组8只大鼠(n=8)。线栓法建立大鼠脑缺血模型,多排螺旋CT灌注成像测量脑血流动力学参数,采用还原型尼克酰胺腺嘌呤二核苷酸黄递酶(NADPH-d)法,观察脑缺血后NOS表达规律及其演变过程。结果正常对照组大鼠尾壳核NOS阳性神经元平均细胞数为(16.63±2.07)个/mm2。缺血1 h NOS阳性神经元数量增加,平均数为(21.63±1.30)个/mm2,与对照组比较,有统计学意义(P<0.05)。缺血6 h NOS阳性神经元数量明显下降,均数是(1.63±1.06)个/mm2,与对照组及缺血1 h组比较,缺血侧NOS神经元数量明显减少,具有统计学意义(P<0.05)。缺血24 h NOS阳性神经元数量进一步减少并几乎消失,均数为(0.50±0.53)个/mm2。结论CT灌注成像有利于观察脑缺血后NOS阳性神经元变化情况。
Objective To observe the expression of nitric oxide synthase (NOS) in the caudate putamen of rats with severe focal cerebral ischemia and provide anatomic evidence for the pathogenesis of cerebral ischemia. Methods Forty SD rats were randomly divided into five groups: (1) normal control group, (2) sham operation group, (1) cerebral ischemia 1 h group, (4) cerebral ischemia 6 h group, (5) Cerebral ischemia 24 h group. Eight rats per group (n = 8). The rat model of cerebral ischemia was established by thread occlusion method. The hemodynamic parameters were measured by multislice spiral CT perfusion imaging. NADPH-d was used to observe the changes of cerebral ischemia Post NOS expression and its evolution. Results The average number of NOS positive neurons in the caudate putamen was (16.63 ± 2.07) / mm2 in normal control rats. The number of NOS positive neurons increased at 1 h after ischemia, with an average of (21.63 ± 1.30) / mm2, which was statistically significant compared with the control group (P <0.05). The number of NOS positive neurons decreased significantly at 6 h after ischemia, with a mean of (1.63 ± 1.06) / mm2. Compared with the control group and the ischemia 1 h group, the number of NOS neurons in the ischemic side decreased significantly, with statistical significance ( P <0.05). After 24 h of ischemia, the number of NOS positive neurons further decreased and almost disappeared with a mean of (0.50 ± 0.53) / mm2. Conclusion CT perfusion imaging is conducive to observe the changes of NOS positive neurons after cerebral ischemia.