七氟烷后处理减轻大鼠局灶性脑缺血-再灌注损伤与黄嘌呤氧化酶

目的：探讨七氟烷后处理减轻大鼠局灶性脑缺血-再灌注（I／R）损伤中黄嘌呤氧化酶（xanthine oxidase，XO）含量变化的意义。方法：40只SD大鼠，随机入假手术（Sham）组、缺血-再灌注（I／R）组、七氟烷后处理（PostS）组．IR＋别嘌醇（Adenock A,I／R＋A）组。各10只。大脑中动脉线栓（MCAO）法建立大鼠局灶性脑缺血损伤模型。观察缺血前、再灌注后各组血清XO．超氧化物岐化酶（SOD）活性．丙二醛（MDA）含量及脑组织Na^＋-K^＋-ATP酶（Na^＋-K^＋-ATPase）活性变化。实验结束后，处死大鼠。取脑组织经HE．TTC染色，观察各组脑组织梗死体积。结果：再灌注24h末，Sham组血清XO活性，MDA含量低于其它三组（p〈0．05）。SOD及脑组织Na^＋-K^＋-ATPase活性高于其它三组（p〈0．05）：I／R组与Posts组、I／R＋A组比较．XO活性升高（p〈0．05），MDA含量增加（p〈0．05），SOD、Na＋^-K^＋-ATPase活性降低（p〈0．05）；S组SOD、XO以及Na^＋-K^＋-ATPase活性均高于IR＋A组（p〈0．05）．MDA含量低于IR＋A组（p〈0．05）。结论：下调XO活性。可能是七氟烷后处理有效减轻大鼠脑缺血-再灌注损伤重要途径之一。

The Effect of Xanthine Oxidase in Post-conditioning of Sevoflurane on Cerebral Infarction Volume in Focal Cerebral Ischemia/Reperfusion Rat Mode

To explore the significance of change in xanthine oxidase content in rat＇s focal cerebral ischemia/reperfusion injury, that was treated with sevoflurane post-conditioning. Method： 40 healthy SD rats, with either sex, were randomly divided into 4 groups： shame group,ischemia/reperfusion injury （I/R） group, postcondition with sevoflurane （PostS） group, I/R plus Adenock（A） （I/R＋A） group, 10 in each. Focal cerebral ischemia/reperfusion model was established in wistar with suture method. The activities of superoxide dismutase（SOD）, xanthine oxidase （XO） , malondialdehyde（MDA） and sodion-potasium ion-dependant triphophade adenosin enzyme （Na^＋-K^＋-ATPase） were measured, volume of cerebral infarction determined with dyeing by hematoxylin eosin （HE） and triphenyltetrazolium staining（TTC） at the end of reperfusion. Result： The activities of XO, MDA, SOD and Na^＋-K^＋-ATPase are much higher in sham group than that of I/R, PostS and I/R＋A groups （p〈0.05） at the end of reperfusion. The volume of cerebral infarction is much less in PostS than that of I/R＋A group （p〈0.05） . Conclusion： Post-conditioning with sevoflurane can attenuate ischemia/reperfusion injury in rat＇s focal cerebral infarction, descending the activity of XO maybe one of the important ways.