摘要
目的探讨超氧化物歧化酶(SOD)在缺血前和缺血后丙泊酚联合应用保护兔脊髓缺血再灌注损伤(SCIRI)中的相对作用。方法 60只日本大白兔采取随机数字表双盲均分为三组:假手术组(S组)、缺血再灌注组(I/R组)、丙泊酚保护组(P组)。S组只行手术操作,不阻断主动脉;I/R组和P组采取主动脉阻断40min成功建立SCIRI损伤模型;P组于主动脉阻断前10min和再灌注即刻分别以微量泵持续静脉泵注丙泊酚(30mg/kg溶于30ml生理盐水,输注速度3ml/min),其余两组在相同时间点则以相同的容量、速度泵注生理盐水。三组动物分别于术后2h、1d、2d、3d、5d、7d行后肢神经功能评分,并于术后1d、2d、3d、5d、7d均处死4只动物,取脊髓组织,检测脊髓组织SOD1、SOD2活性和病理学评判。结果 (1)同一时间点(2h、1d、2d、3d)三组动物后肢神经功能评分和脊髓组织病理切片分级两两比较,差异均有统计学意义(均P<0.01)。(2)三组动物SOD1活性组内比较:I/R组术后第1天,SOD1活性显著增强(P<0.05);S组和P组组内比较差异均无统计学意义(P>0.05)。三组动物组间比较:术后第1天,与S组比较,I/R组和P组SOD1活性均显著增强(均P<0.05);第2天、第3天,与S组比较,P组SOD1活性仍显著增强(P<0.05);第5天,与I/R组比较,P组SOD1活性仍然升高(P<0.05)。(3)三组动物SOD2活性组间比较,术后第1天、第2天、第3天、第5天、第7天,与S组比较,I/R组SOD2活性均显著降低(P<0.05)。结论缺血前和缺血后丙泊酚联合应用可以保护兔SCIRI,保护作用机制可能是丙泊酚通过其内源性抗氧化作用,提高了脊髓组织中SOD1的活性,而与脊髓组织中SOD2活性的表达无直接相关性。
Objective To investigate the relative effect of superoxide dismutase （SOD）in combined application of propofol preconditioning and postconditioning on spinal cord injury induced by ischemia-reperfusion in a rabbit model. Methods Sixty Japanese rabbits were randomly divided into 3 groups ： sham-operation group （ group S） ;ischemia-reperfusion group（ group I/R） ;ischemia-reperfusion group with propofol treatment （group P）. Group S only dealed with surgical operation but no aortic cross-clamp, while spinal cord ischemia was induced by infra-renal aortic cross-clamp for 40 minutes in group I/R and group P and established the SCIRI injury model successfully. Propofol was intravenously infused at 30 mg/kg in 30 ml 0.9% sodium chloride at the speed of 3 ml/min in group P for two times,once at 10 minutes before aortic clamping and once at the onset of reperfusion. Other two groups were managed with the same capacity of 0. 9% sodium chloride at the same time. Neurological functions were evaluated at 2 h,1 d,2 d,3 d,5 d,7 d after operated. Every 4 animals were killed at lst,3rd,5th,7th day after management. The spinal cord tissues were eviscerated and we detect the bioactivity of its SOD1, SOD2 and carry out evaluation mean of pathological slices. Results （1）The differences were statistically significant in neurological function scores and evaluation of pathological slices （ P 〈 0.01 ）. （2） Within each group of animals, the bioactivity of SOD1 aggrandized observably in group I/R（P 〈 0.05）, while it was unchangeable in group S and group P （ P 〉 0. 05 ）. Compared withgroup S, the bioactivity of SOD1 increased significantly in group/JR and group P（ P 〈 0. 05） at ld, which sustained in group P at 2 d and 3 d after operation. Meanwhile, the bioactivity of SOD1 increased significantly in group P at 5 d after operation compared with group I/R （ P 〈 0. 05 ）. （ 3 ） The bioactivity of SOD2 of group I/R decreased significantly compared with group S （P 〈 0. 05 ）. Conclusions Combined application of propofol preconditioning and postconditioning show potently protective effects against the spinal cord ischemia reperfusion injury in the rabbit model. The mechanisms may be that propofol increases the bioactivity of SOD1 in the spinal cord tissue, and there is no correlation directly with the bioactivity of SOD2.
出处
《中华临床医师杂志（电子版）》
2013年第2期130-134,共5页
Chinese Journal of Clinicians(Electronic Edition)
基金
湖北省卫生厅青年人才基金(QJX2010-14)
