脊髓组织缺血再灌注早期MDA及SOD动态变化.docVIP

脊髓组织缺血再灌注早期MDA及SOD动态变化 　【摘要】 目的 研究脊髓缺血再灌注早期脊髓组织丙二醛（malonyldialdehyed,MDA）含量及超氧化物歧化酶（superoxide dismutas,SOD）活性变化，探讨自由基在脊髓继发性损伤中的作用。方法 48 只成年雄性SD大鼠采用腹主动脉肾动脉下方夹闭法造成脊髓缺血再灌注模型，连续观察再灌注后1h、6h、12h、18h、24h脊髓组织内MDA和SOD活性。结果 脊髓缺血再灌注后脊髓组织MDA立即上升，6h达最高峰，此后随之下降，但至24h仍高于正常对照组；SOD活性显著下降，6h达最低，随后逐渐回升，至24h基本接近缺血前。结论 MDA和SOD参与了脊髓缺血再灌注继发性损伤的病理过程。 【关键词】 缺血再灌注；自由基；超氧化物歧化酶； 动物，实验；丙二醛 　　ABSTRACT Objective To study the early content changes of malonyldialdehyed (MDA) and the early activity changes of superoxide dismutas (SOD) after spinal cord ischemia reperfusion, and to discuss the effect of free radical in spinal cord secondary injuries. Methods Abdominal aortic corss-clamping was performed in 48 adult male Sprague-Dawley (SD) rats to get the spinal cord ischemia reperfusion model; the content of MDA and the activities of SOD in spinal cord were measured 1h, 6h, 12h, 18h and 24h after reperfusion.Results The content of MDA increased immediately after reperfusion and reached the peak 6h after reperfusion, then it started decreasing, but it was still higher than that of the control 24h after reperfusion; the activities of SOD decreased obviously after reperfusion and reached the lowest level 6h after reperfusion, then they started ascending and 24h after reperfusion, they recovered to the level before reperfusion.Conclusions MDA and SOD participate in the pathological process of the secondary injury of spinal cord ischemia reperfusion. 　　KEYWORDS ischemia reperfusion free radical superoxide dismutas animal experiment malonyldialdehyed 　　 　　临床常见的脊柱骨折、脊髓供血动脉疾患、脊髓内显微外科手术、骶管肿瘤手术、主动脉瘤手术甚至麻醉操作等常导致脊髓缺血而引起截瘫的发生。在这一过程中，除缺血缺氧对脊髓直接损害外，血流恢复后自由基对脊髓的继发性损伤亦起了重要作用［1］。本实验观察了脊髓缺血再灌注早期脊髓组织内丙二醛（malonyldialdehyed,MDA）含量及超氧化物歧化酶（superoxide dismutas,SOD）活性的变化规律，以探讨脊髓继发性损伤的病理机制。 　　1 材料与方法 　　1．1 动物分组及模型建立 　　48只健康成年雄性SD大鼠，体重200～250g，随机分为缺血前（假手术组）、缺血再灌注后1h、6h、12h、18h、24h组，共6组，每组8只。所有动物均经腹腔注射1%戊巴比妥钠（60mg/kg）麻醉，麻醉后常规消毒，左侧腹部背最长肌外侧缘直切口，解剖分离腹主动脉,于左肾动脉下方夹闭腹主动脉40min，然后开放腹主动脉，关闭腹腔，造成脊髓缺血再灌注模型。缺血前组除不夹闭腹主