硫酸镁对兔脊髓缺血再灌注损伤的保护

背景硫酸镁用于脑缺血再灌注损伤的治疗已取得了较满意的疗效,但对脊髓缺血再灌注损伤的作用机制尚不十分清楚.目的观察硫酸镁对兔脊髓缺血再灌注损伤的保护效果,进一步探讨其作用机制.设计以实验动物为研究对象,随机对照的重复测量设计.单位一所大学医学院中心实验室.对象实验于2003-04/2004-06在西安交通大学医学院中心实验室完成.健康成年新西兰大白兔27只,体质量1.9～2.5 kg.随机抽签法分为硫酸镁组、生理盐水组和假手术组,每组9只.方法夹闭腹主动脉肾下段30min后恢复血流再灌注48 h,建立兔脊髓腰骶段缺血模型.硫酸镁组给予静脉灌注硫酸镁(0.25 mL/kg·h),生理盐水组用等量生理盐水代替.假手术组仅行中线剖腹术,不结扎动脉.在缺血前,缺血30 min及再灌注后1,2,8,16,24 h对动物行体感诱发电位监测,再灌注24及48 h后对硫酸镁组、生理盐水组动物行运动功能评分.再灌注后48 h处死动物,对脊髓行组织病理学检查.主要观察指标①运动功能评分.②体感诱发电位监测.③脊髓组织病理学检查.结果缺血30 min时硫酸镁组体感诱发电位(N1)潜伏期明显延长;再灌注后前2 h潜伏期较缺血时明显恢复,其后又显著延长.缺血30 min时生理盐水组波形消失.假手术组体感诱发电位没有明显变化,动物均完全康复.硫酸镁组各时间点潜伏期恢复均明显高于生理盐水组(P＜0.05);再灌注24和48 h后,硫酸镁组的神经功能评分分别为(3.7±0.5)和(3.4±0.7)分,均显著高于生理盐水组(3.0±0.7)和(2.6±0.9)分](P＜0.05);再灌注48 h后硫酸镁组的脊髓前角正常神经细胞计数显著高于生理盐水组(23.4±3.4,12.3±3.2,P＜0.01).结论硫酸镁具有减轻兔脊髓缺血再灌注损伤及保护神经功能的作用.

Magnesium sulfate for spinal cord ischemia-reperfusion injury in rabbits

BACKGROUND: It has been reported that magnesium sulfate(Mg2SO4)treatment has a satisfactory effect on brain ischemia-reperfusion injury, but its effect on spinal cord ischemic injury remains unclear.OBJECTIVE: To evaluate the effects of intravenous administration of Mg2SO4 on spinal cord ischemia-reperfusion injury and further probe into its mechanism.DESIGN: Randomized controlled repeatedly measuring design based on the experimental animals.SETTING: Central research laboratory of a university hospital.MATERIALS: The experiment was conducted in the Central Research Laboratory, Medical College of Xi' an Jiaotong University from April 2003 to June 2004. Twenty-seven New Zealand white rabbits with body mass of 1.9to 2. 5 kg were included. The rabbits were randomly divided into Mg2SO4group, normal saline group and sham-operation group with 9 rabbits in each group.METHODS: The lower segment of the kidney under abdominal aorta was occluded for 30 minutes and 48-hour reperfusion was performed to establish ischemia-reperfusion model of lumbosacral segment of spinal cord. Mg2SO4group (Group A, n = 9) received Mg2SO4 at the dose of 0. 25 mL/kg per hour throughout this procedure; the same volume of saline solution was used in normal saline group(Group B, n=9) . Animals of sham-operation group (Group C, n = 9) were anesthetized and received laparotomy without aortic occlusion. The somatosensory evoked potential(SEP) was detected before ischemia, 30 minutes after ischemia, and 1, 2, 8, 16 and 24 hours after reperfusion. Motor function score was assessed in Mg2SO4 and saline groups 24 and 48 hours after reperfusion. After reperfusion for 48 hours, the animals were killed and histopathological test was performed on the spinal cord.MAIN OUTCOM MEASURES: Motor function score, SEP monitoring and spinal histopathological test.RESULTS: The latency of SEP(Nt) was markedly longer 30 minutes after ischemia in Mg2SO4 group. It was obviously recovered during the first two hours after reperfusion compared with during ischemia, but was obviously prolonged after that. Waveform disappeared 30 minutes after ischemia in normal saline group. SEP amplitudes and latencies in sham-operation group did not change remarkably during the procedures and all the animals recovered without neurological deficits. At each reperfusion time point, the recovery of SEP(N1) latency was better in Group A than that in Group B( P ＜ 0.05). The average motor function score at 24 hours and 48 hours after reperfusion was significantly higher in Group A (3.7 ±0.5) and(3.4 ±0.7) points] than that in GroupB (3.0±0.7) and (2.6±0.9) points](P ＜0.05). The normal nerve cell counting of spinal cord 48 hours after reperfusion in Mg2SO4 group(23. 4 ± 3. 4) was significantly higher than that in saline group (12.3 ±3.2)(P ＜ 0.01).CONCLUSION: Intravenous Mg2SO4 administration may reduce spinal cord injury and preserve neurological function in transient spinal cord ischemia in rabbits.