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目的 以大鼠迟发性脑血管痉挛模型为基础研究诱导型一氧化氮合成酶 (iNOS)在迟发性血管痉挛发展中的作用。方法 3 2只雄性SD大鼠随机分为实验组和对照组 ,实验组枕大池二次注血诱导迟发性脑血管痉挛 ,对照组枕大池注射生理盐水。第 8天行脑血管造影 ,枕大池抽取脑脊液测一氧化氮 (NO)浓度。逆转录 聚合酶链反应 (RT PCR )法和免疫组织化学法测定并评价iNOSmRNA和蛋白质在基底动脉、大脑中动脉和皮质中的表达。结果 颅内动脉血管减影提示对照组颈内动脉颅内段、大脑中动脉 (MCA)明显变细 ,大脑中动脉中段直径 (MD)与镫骨动脉中段直径 (SD)之比衡量大脑中动脉的管径显示实验组MCA管径较对照组MCA管径减少 3 0 %。对照组脑脊液中NO浓度为 (11.70± 2 .62 ) μmol/L ,实验组脑脊液中NO的浓度为(5 5 .67± 12 .84)μmol/L。iNOSmRNA和蛋白质表达于基底动脉、大脑中动脉和皮质 ,其中基底动脉表达最强。 结论 iNOS作为迟发性脑血管痉挛发展中的关键因素参与血管壁的迟发性损伤。
Objective To study the role of inducible nitric oxide synthase (iNOS) in the development of delayed vasospasm in rats with delayed cerebral vasospasm. Methods Three male Sprague - Dawley rats were randomly divided into experimental group and control group. Experimental group received secondary injection of occipital cisternae to induce delayed cerebral vasospasm, and saline into control group. Cerebral angiography was performed on day 8, and cerebrospinal fluid (CSF) was collected for determination of nitric oxide (NO) concentration. Reverse transcription polymerase chain reaction (RT PCR) and immunohistochemistry were used to determine the expression of iNOS mRNA and protein in basilar artery, middle cerebral artery and cortex. Results Intracranial angiography showed that the ratio of MCA to MCA in the control group was significantly smaller than that in the middle cerebral artery (SD) The diameter of the experimental group showed that the MCA diameter decreased by 30% compared with that of the control group. The concentration of NO in cerebrospinal fluid of the control group was (11.70 ± 2.62) μmol / L, and that of the experimental group was (55.76 ± 12.84) μmol / L. The iNOS mRNA and protein were expressed in the basilar artery, middle cerebral artery and cortex, of which basilar artery was the most expressed. Conclusion iNOS participates in the delayed injury of vascular wall as a key factor in the development of delayed cerebral vasospasm.