脑缺血再灌注大鼠海马CA1区线粒体功能与氧自由基产生的关系

Relation of mitochondrion function in hippocampal CA1 region with produce of oxygen free radical during cerebral ischemia reperfusion

目的:探讨缺血再灌注过程中线粒体功能变化及其与氧自由基产生的关系。方法:采用颈动脉分流法制备大鼠脑缺血再灌注模型,测定海马CA1区线粒体ATP合成能力、呼吸功能及此区组织丙二醛含量的变化。结果:线粒体ATP合成能力在再灌注12h及12～24h下降最快,与其他组比较差异有显著性意义(t=3.25～4.26,P<0.05),呼吸四态的氧消耗率在再灌注12,24,36,48h后逐渐上升,与假手术组及缺血5min组相比差异有显著性意义(t=5.32～5.74,P<0.05)。再灌注24～36h,36～48h其上升最快,与其他组比较差异有显著性意义(t=5.56,5.74,P<0.05)。此区组织丙二醛在再灌注24h前逐渐上升且在24h犤(398.6±5.3)nmol/g犦达到高峰。再灌注36,48h组织内丙二醛含量逐渐下降,但仍高于假手术组丙二醛含量犤(256.9±9.6)nmol/g犦(t=3.23～4.56,P<0.05)。结论:海马CAl区组织再灌注早期(24h之前)氧自由基产生主要通过组织途径,24h之后则是组织途径与呼吸链途径共同作用的结果。

AIM:To study the association between the changes of mitochondrion function and the product of oxygen free radicals during cerebral ischemia reperfusion. METHODS:Rat model of cerebral ischemia reperfusion was established by using ca rotid bypass method so as to detect the capacity of mitochondrion producing ATP in hippocampal CA1 region,respiratory capacity of mitochondrion and the change o f malonic dialdehyde(MDA) content. RESULTS:The capacity of mitochondria producing ATP decreased fastest during th e first 24 hours of reperfusion, showing significant differences as compared wit h other groups(t=3.25-4.26,P< 0.05).The oxygen consumption rate of respiration -4-condition had a remarkable increase 12 hours after reperfusion, and had a s ignificant difference from that in the sham operation and ischemia for 5 minutes groups(t=5.32-5.74,P< 0.05). The oxygen consumption rate was increased fastest at 24-36 and 36-48 hours after reperfusion, with significant difference(t=5.5 6,5.74,P< 0.05).In addition, the content of MDA increased gradually into the pea k [(398.6±5.3) nmol/g] at 24 hours,and then began to decrease at 36-48 hours a fter reperfusion, but was still higher than that in the sham operation group[(25 6.9±9.6) nmol/g](t=3.23-4.56,P< 0.05). CONCLUSION:The product of oxygen free radicals is mainly dependent on the path way of tissue before 24 hours of reperfusion in hippocampal CA1 region,and then results from the combination action of tissue and respiratory chain pathway.