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硫酸镁对弥漫性脑损伤脑组织的保护作用及机制
引用本文:李玉,潘延成,朱贤立. 硫酸镁对弥漫性脑损伤脑组织的保护作用及机制[J]. 中华实验外科杂志, 2009, 26(8). DOI: 10.3760/cma.j.issn.1001-9030.2009.08.033
作者姓名:李玉  潘延成  朱贤立
作者单位:1. 河南省人民医院神经外科,郑州,450003
2. 山东省滕州市中心人民医院
3. 华中科技大学同济医学院附属协和医院
摘    要:目的 探讨硫酸镁对于弥漫性脑损伤脑组织可能的保护机制.方法 依据Marmarou's弥漫性脑损伤动物模型有改进,采用成年健康SD雄性大鼠,体质量325~375 g,共50只.其中,外伤组25只,干预组25只(两组外伤后12、24、48、72 h,1周,每组各5只).干预组应用微泵给予硫酸镁静脉注射治疗,外伤后大鼠自由进食水,按时间段处死大鼠,提取大鼠皮层脑组织,应用实时逆转录.聚合酶链反应(realtime RT-PCR)检测外伤组与干预组不同时间段ET-1 mRNA、iNOS mRNA表达,另取脑组织应用脑组织干湿重比表示脑组织含水量.结果 ET-1 mRNA表达干预组较外伤组干预组降低,应用成组t检验分析方法检验可得:6、12、24、48 h组组间差异有统计学意义(P<0.01),72 h,1周组间比较差异无统计学意(P>0.05).iNOS mRNA表达干预组较外伤组降低,干预组与外伤组相应时间组组间差异有统计学意义(P<0.01).结论 应用微泵静脉注射硫酸镁早期减少了ET-1 mRNA、iNOS mRNA的表达,从而使ET-1、iNOS、NO合成减少,减轻了脑组织缺血缺氧及对脑细胞的毒性,从而使干预组弥漫性脑损伤大鼠脑组织含水量较单纯外伤组弥漫性脑损伤大鼠脑组织含水量减少的原因.

关 键 词:脑损伤  硫酸镁

The protective effects of magnesium sulfate on diffuse brain injury and the undergoing mechanism
LI Yu,PAN Yan-cheng,ZHU Xian-li. The protective effects of magnesium sulfate on diffuse brain injury and the undergoing mechanism[J]. Chinese Journal of Experimental Surgery, 2009, 26(8). DOI: 10.3760/cma.j.issn.1001-9030.2009.08.033
Authors:LI Yu  PAN Yan-cheng  ZHU Xian-li
Abstract:Objective To investigate the protective mechanism of magnesium sulfate against diffuse brain injury (DBI).Methods Fifty male SD rats were randomly divided into two groups:control group (pure DBI, being divided into 5 subgroups, n = 5 each), therapeutic group (being divided into 5 subgroups,n =5 each).The expression of ET-1 and iNOS mRNA was detected by realtime RT-PCR in two groups.The water content in brain was determined after pure DBI or treatment.Results The expression of ET-1 and iNOS mRNA in therapeutic group was lower than in control groups with the difference being sig-nificant at the same time point between two groups by t test.The water content in brain of therapeutic group was decreased as compared with control group at the same time point.Conclusion After intravenous injection of magnesium sulfate,the expression of ET-1 and iNOS mRNA following DBI was downregulated, and the water content in brain following DBI was declined, by which the edema of the damaged brain was declined.
Keywords:ET1  iNOS
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