脊髓缺血再灌注损伤后神经功能修复的实验研究

An experimental study of neuronal function restoration following ischemic reperfusion injury of spinal cord

目的 研究青紫兰兔脊髓缺血 40min和再灌注 4h脊髓组织兴奋性氨基酸 (EAAs)和细胞内Ca2 + ([Ca2 + ]i)的含量变化 ,及其EAAs受体拮抗剂氯胺酮对上述指标的影响。 方法 健康青紫兰兔 30只 ,随机均分为手术对照组、缺血 40min组、再灌注 4h组、氯胺酮 +硫酸镁治疗组、氯胺酮治疗组、等渗盐水治疗组。测定脊髓组织中谷氨酸 (GLU)、天门冬氨酸 (ASP)及 [Ca2 + ]i含量。同时观察氯胺酮、硫酸镁对上述指标的影响。 结果 缺血 40min组 ,GLU和ASP含量明显降低 ,分别为 (15 .18± 2 .33) μmol g和 (9.99± 0 .6 9) μmol g ;再灌注 4h组 ,GLU和ASP含量降低更加明显 ,分别为 (13.75± 2 .5 8) μmol g和 (6 .49± 1.39) μmol g ;同时 [Ca2 + ]i含量在缺血 40min时有所升高 [(2 2 1.2± 4.2 7) μg g],再灌注 4h组则较缺血 40min组升高更加明显 [(2 98.3± 9.2 6 ) μg g]。氯胺酮能明显升高缺血再灌注期GLU和ASP含量 ,分别为 (2 1.5 1± 5 .42 ) μmol g和 (9.5 5±2 .45 ) μmol g,并将 [Ca2 + ]i含量显著降低至 (2 18.6± 7.0 8) μg g。 结论 EAAs的兴奋性神经毒性作用及其所引起的Ca2 + 超载在脊髓缺血再灌注损伤中发挥着至关重要的作用 。

Objective To study the content varies of excitatory amino acids (EAAs)and intracellular calcium([Ca 2+ ]i)of spinal cord tissues from lumbar spinal cord in rabbits after 40 minutes of ischemia and 4 hours of reperfusion, and to observe the effects of the EAAs receptor antagonists ketamine on aforementioned targets. Methods Thirty healthy rabbits were divided into 6 groups: sham operation, 40 minutes of ischemia, 4 hours of reperfusion, 4 hours of reperfusion treatment with ketamine, MgSO 4 and physiological saline groups. The contents of EAAs (glutamate and aspartate) and [Ca 2+ ]i were measured. In addition, the effects of ketamine and MgSO 4 on aforementioned targets were observed in these rabbits. Results The results revealed that in group of 40 minutes after ischemia, the GLU and ASP contents of the EAAs transmitterswere decreased to (15.18±2.33) μmol/g, (9.99±0.69) μmol/g differently,and further to (13.75±2.58) μmol/g, (6.49±1.39) μmol/g after reperfusion. But after 40 minutes of ischemia, [Ca 2+ ]i was elevated to (221.2±4.27)μg/g, and further to (298.3±9.26) μg/g after the reperfusion, which were more significantly than that of ischemia and control groups. Ketamine could increase obviously the level of GLU and ASP to (21.51± 5.42 ) μmol/g and (9.55±2.45) μmol/g, and decrease the [Ca 2+ ]i to (218.6±7.08) μg/g during the ischemia and reperfusion. Conclusions The study proves that the excitotoxicity of EAAs and the overload of calcium induced by EAAs play an important role in spinal cord ischemia reperfusion injury. Ketamine demonstrates an effective restrained role to the injury mechanism and has a good prospect.