摘要
目的 观察一氧化氮（NO）含量的变化对大鼠局灶性脑缺血再灌注损伤后脂质过氧化的影响。方法 采用线栓法制作大鼠局灶性脑缺血再灌注损伤模型，应用Griss反应法测定脑组织NO含量变化，微量测定法测定超氧物歧化酶（SOD）活性和脂质过氧化产物丙二醛以及NO合酶（NOS）抑制剂NG-硝基-左旋精氨酸甲酯（L-NAME）对它们的影响。结果 脑缺血1 h再灌注1 h脑组织匀浆中NO2-含量升高，SOD活性降低，丙二醛（MDA）含量明显升高，与假手术组比较P<0.01；L-NAME能部分抑制SOD活性的降低及NO2－、MDA含量的升高，与生理盐水治疗对照组比较，P<0.01。结论 小剂量NOS抑制剂能减轻急性脑缺血再灌注损伤脂质过氧化损伤。
Objective To explore the effects of nitric oxide on lipid peroxidation in the rat brain during reperfusion after focal cerebral ischemia. Methods Focal cerebral ischemia-reperfusion model was made by means of intralumin filament. The concentration of nitric oxide (NO) in the brain tissue was measured using Gress' method. The activity of superoxide dismutase (SOD) and the concentration of malondialdehyde (MDA) were determined by using microassay. Results There was a significant increase in the levels of NO product and MDA at 1 h of reperfusion after occlusion of the middle cerebral artery for 1 h. Administration of low-dose nitrin oxide synthase inhibitor, NG-nitro-L-arginine methy ester (L-NAME), prior to reperfusion significantly decreased the levels of NO product and MDA. Conclusion These results indicate that NO plays an important role in the neuronal injury after cerebral inchemic-reperfusion, and the inhibition of NO synthase activity protects against lipid peroxidation during reperfusion after focal cerebral ischemia.
出处
《第一军医大学学报》
CSCD
2000年第3期242-244,共3页
Journal of First Military Medical University
