摘要
目的观察丙泊酚对大鼠脑缺血-再灌注损伤后海马线粒体三磷酸腺苷(ATP)含量、ATP酶活性、脂质过氧化和超微结构的影响。方法采用大鼠全脑缺血-再灌注损伤模型。40只Wistar大鼠随机分为假手术组(A组)、缺血-再灌注对照组(B组)和缺血-再灌注丙泊酚预处理组,后者按丙泊酚用量又分为50 mg/kg(C1组)1、00 mg/kg(C2组)和150 mg/kg(C3组)三个亚组。观察全脑缺血10 min再灌注60 min时海马线粒体的超微结构、ATP和丙二醛(MDA)的含量及Na+-K+-ATP酶、Ca2+-ATP酶、超氧化物歧化酶(SOD)和谷光甘肽(GSH)活性的变化。结果与B组比较,丙泊酚各处理组海马线粒体的ATP含量、Na+-K+-ATP酶、Ca2+-ATP酶、SOD和GSH的活性均有不同程度的增高(P<0.05或0.01),MDA含量有不同程度的降低(P<0.05或0.01),线粒体超微结构的损伤程度亦明显减轻。结论丙泊酚对脑缺血-再灌注损伤的保护效应可能与其抑制线粒体脂质过氧化反应,减轻线粒体的损伤,促进线粒体ATP含量和ATP酶活性的恢复有关。
Objective To investigate the effects of propofol on the ATP content,ATPase activity,lipid peroxidation and ultrastructure in the hippocampus mitochondrial in global ischemia-reperfusion rats. Methods The rat model of global ischemia-reperfusion was established by Pulsinelli 4-vessel occlusion method. Forty male Wistar rats were ramdomly allocated into five groups with eight animals each. Group A,as a sham operation group, was given normal saline 5ml ip at the end of operation. Group B,as an ischemia-reperfusion control,was given normal saline 5 ml ip 10 min before ischemia; and group C1 ,C2 and C3 were treated with propofol 50 mg/kg, 100 mg/kg and 150 mg/kg ip 10 min before ischemia respectively. After global ischemia for 10 min and reperfusion for 60 min,the rats were decapitated and the hi ppocampus was removed. The contents of ATP, ADP, AMP and MDA,activities of Na^＋-K^＋-ATPase, Ca^2＋ -ATPase, SOD and GSH in the hippocampus mitochondrial were measured. and mitochondrial structure was observed using electron microscope. Results The contents of ATP, ADP and AMP, activities of Na^＋-K^＋-ATPase, Ca^2＋-ATPase, SOD and GSH decreased significantly and the content of MDA increased obviously in group B than those in the other groups. Electron microscopic examination also showed that there were severe mitochondria edema and degeneration in group B,and the damages were milder in group C1-C3 than those in group B. Conclusion Neuroprotective effects of propofol may be related to inhibiting mitochondrial lipid peroxidation, reducing the changes of mitochondrial structure,and improving the mitochondrial energy metabolism and ATPase activity after global ischemia-reperfusion.
出处
《临床麻醉学杂志》
CAS
CSCD
2005年第10期716-718,共3页
Journal of Clinical Anesthesiology
