血钾调整对大鼠脑组织缺血再灌注损伤后氧化应激水平的影响

The Effect of Regulation of Serum Potassium Concentration on the Cerebral Oxidative Stress of Rat with Ischemia/reperfusion Injury

目的:研究改变血钾浓度能否减轻大鼠局灶性脑缺血再灌注损伤(cerebral ischemia-reperfusion in-jury,CIRI)。方法:健康的SD大鼠随机接受大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)手术或者仅分离结扎颈外动脉处理(Sham组,n=16)。接受MCAO手术的动物在120分钟时给予恢复灌注,并随机通过颈静脉泵入3 ml/kg的0.9%生理盐水(NS组,n=16)或3ml/kg的3%氯化钾(potassium chloride,KCl)溶液(KCl组,n=16),走速设定8 ml/h。输液完成5 min后比较三组大鼠的血钾浓度。再灌注24 h后进行神经功能评分,并进行HE染色、检测活性氧(reactive oxygen species,ROS)、丙二醛(malondialdehyde,MDA)水平和总超氧化物歧化酶(total superoxide dismutase,T-SOD)活力。结果:与NS组对比,KCL组动物血钾浓度升高(P<0.01),HE染色提示组织损伤减轻,ROS、MDA水平降低(P<0.05),但是T-SOD水平无组间差异。结论:再灌注时给予KCl调整血钾浓度能够减轻大鼠局灶性脑损伤,其机制可能与氧化应激减弱有关。

Objective ： To investigate whether the change of serum potassium could reduce the cerebral ischemia-re- perfusion injury. Methods： Healthy Sprague-Dawley rats were randomly subjected to middle cerebral artery occlusion （MCAO） or Sham operation （Sham group, n=16）. The rats were subjected to MCAO for 120 min followed by reperfusion and then were randomly administered 3ml/kg normal saline （NS group, n = 16） , 3 ml/kg 3% KC1 solution （KC1 group, n = 16, 90 mg/kg） at a speed of 8 ml/h using micro pump via the fight jugular vein. The rats in the Sham group only underwent the fight vascular exposure 120 min without MCAO （n= 16）.5 rain later, we assessed the serum potassium concentration. And at 24 h after reperfusion, the neural function was assessed. HE staining, reactive oxygen species （ROS）, malondialdehyde （MDA） level and total superoxide dismutase （T-SOD） activity were measured. Results： Compared to the NS group, the serum potassium concentrations in the KC1 group were significantly increased （P 〈 0.01 ）. HE staining showed that the brain sections from the KC1 group presented less neuronal damage. Also, elevated serum potassium could significantly reduce ROS, MDA contents （P 〈 0.05）, although, there was no significantly difference between NS group and KC1 group. Conclusion： Elevated serum potassium could attenuate oxidative stress induced by cerebral IR.