摘要
【目的】通过观察左卡尼汀大鼠对心肺复苏后脑组织丙二醛（MDA）、超氧化物歧化酶（SOD）含量及神经细胞凋亡的变化，探讨左卡尼汀对复苏后脑神经细胞保护作用的机制。【方法】建立心肺复苏大鼠模型，90只Wistar大鼠随机分为手术对照组（S组）、常规复苏组（C组）和左卡尼汀组（L组），每组30只，S组只行手术操作，不致颤；C组造成心搏骤停并行常规复苏；I。组在心搏骤停并复苏成功后静脉注射左卡尼汀。动态观察脑组织丙二醛（MDA）、超氧化物歧化酶（SOD）含量及海马回神经细胞凋亡的变化。HE染色观察大鼠脑组织的病理改变。【结果】与S组比较，C组和L组复苏成功后脑组织MDA及凋亡神经细胞数有不同程度升高（P〈0．01），SOD有不同程度下降（P〈0．01）。L组与同时相C组比较，脑组织MDA及凋亡神经细胞数升高程度减轻（P〈0．05），SOD下降程度减轻（P〈0．05），光镜下脑组织损害减轻。【结论】左卡尼汀对大鼠心肺复苏后脑神经细胞氧自由基损伤有保护作用，这可能与左卡尼汀提高脑组织中抗氧化酶活性、抑制氧自由基产生及脂质过氧化反应有关。
[ Objective] To observe the changes of malondialdehyde （ MDA）, superoxide dismutase （SOD） and nerve cell apoptosis of brain tissue in rats treated by levocarnitine after cardiopulmonary resuscitation （CPR） and explore the mechanism of neuroprotective effects of levocarnitine. [Methodsl Rat model of CPR was established. Ninety Wistar rats were randomly divided into operation-control group（group S, n = 30）, routine resuscitation group（group C, n =30） and levocarnitine group（group L, n =30）. Group S was only performed the operation but not induced cardiac arrest. Group C was performed standard CPR after cardiac arrest. Group L was given intravenous injection of levocarnitine after CPR of cardiac arrest. The changes of MDA, SOD and apoptosis in nerve cells of gyrus hippocampi were observed dynamically. HE staining was used to observe the pathological change of brain tissue in rats. [ResultsI Compared with group S, MDA and the number of apoptotic cells in brain tissue after CPR gradually increased and the level of SOD in brain tissue gradually decreased in group C and group L（all P （0.01）. Compared with group C at the same stage, the in- creasing of MDA and apoptotic ceils in brain tissue alleviated（ P 〈0.05）, and the decreasing of SOD in brain tissue reduced（ P 〈0.05）, and brain damage under light microscope relieved in group L. [ConclusionlLevoc-arnitine has the neuroprotective effect against oxygen radical injury of brain nerve cells after CPR. It may be related to the ability of levocarnitines for increasing the antioxidase activity and inhibiting the production of oxygen radicals and lipid peroxidation in brain tissue.
出处
《医学临床研究》
CAS
2011年第11期2036-2040,共5页
Journal of Clinical Research
基金
辽宁省科学技术基金（2009225040）
