依达拉奉对脓毒血症时血及心肌超氧化物歧化酶、黄嘌呤氧化酶的影响

Effects of edaravone on superoxide dismutase and xanthine oxidase in blood and myocardium during sepsis： experiment with rats

目的观察依达拉奉对脓毒血症时血及心肌超氧化物歧化酶（SOD）、黄嘌呤氧化酶（XOD）的影响。方法SD大鼠30只随机均分为假手术组、手术对照组、依达拉奉治疗组。手术对照组和治疗组均予盲肠结扎穿刺法制作脓毒血症模型。三组术前15min及术后3h各皮下注射乳酸左氧氟沙星20mg／kg，治疗组于术前15min及术后3h各皮下注射依达拉奉5mg／kg。各组术后18h采血和取心肌组织测SOD、XOD，并对心肌组织进行组织学检查。结果手术对照组血SOD活力（8．25±3．11）U／ml，显著低于治疗组[（13．20±6．43）U／ml，P〈0．051，两组的血清SOD均显著低于假手术组[（18．21±3．94）U／ml，分别P〈0．01和P〈0．05]。3组间血XOD活力比较无显著性差异（均P〉0．05）。手术对照组心肌细胞SOD活力为（15．22±5．15）U／ml，显著低于假手术组[（21．57±5．82）U／ml，P〈0．05]，治疗组SOD活力为（22．62±7．81）u／ml，与假手术组无显著差异（P〉0．05）。手术对照组心肌细胞XOD活力为（12．86±4．64）U／mg蛋白质，显著高于假手术组[（9．11±2．99）U／mg蛋白质，P〈0．05]）；治疗组心肌细胞XOD活为（8．97±1．22）U／mg蛋白质，显著低于手术对照组（P〈0．05）而与假手术组无显著性差异（P〉0．05）。光镜下可见手术对照组大鼠心肌细胞浊肿，肌束间毛细血管扩张，电镜下可见心肌细胞肌膜轻度水肿，局灶肌丝疏松；光镜下依达拉奉治疗组大鼠心肌组织病变较轻，电镜下心肌细胞肌膜、肌浆网正常。结论依达拉奉能升高血和心肌组织SOD活力及降低心肌组织XOD活力，提高清除自由基和抗氧化能力，具有保护心肌功能作用。

Objective To investigate the effects of edaravone on superoxide dismutase （SOD） and xanthine oxidase （XOD） in blood and myocardium during sepsis. Methods Thirty Sprague-Dawley rats were randomly divided into 3 equal groups： sham operation group, operation control group undergoing caecal ligation and puncture （CLP）, and edaravonc treatment group undergoing subcutaneous injection of 5 mg/＇kg edaravone 15 rain before and 3 h after operation. Subcutaneous injection of 20 mg/kg lactate levofloxacin 15 rain before and 3 h after operation in was given to these 3 groups. Samples of peripheral blood and myocardium were taken from all of the rats 18h after operation to detect the activities of SOD and XOD and observe the pathological changes in the myocardium. Results The activity of SOD in blood of the operation control group was （8.25±3.11） U/ml, significantly lower than that of the treatment group [（ 13.20± 6.43） U/ml, P 〈 0.05]. The activities of SOD in the blood of both groups were both significantly lower than that of the sham operation group [ （ 19.21±3.94） U/ml, P 〈 0.01 and P 〈 0.05]. There were no significant differences among the serum XOD levels of the 3 groups （all P〉0.05）. The myocardium SOD activity of the operation control group was （ 15.22± 5.15 ） U/ml, significantly lower than that of the sham operation group [（21.57±5.82） U/ml, P 〈 0.05], the myocardium SOD activity of the edaravone treatment group was （22.62± 7.81） U/m], not significantly different from that of the sham operation group （P〉 0.05）. The myocardium XOD activity of the operation control group was （12.86±4.64） U /mg protein, significantly higher than that of the sham operation group [（9.11±2.99）U/mg protein, P〈 0.05]. The myocardium XOD activity of the edaravone treatment group was （8.97 ± 1.22）U/mg protein, significantly lower than that of the operation control group （P〈 0.05） and not significantly different from that of the sham operation group （P〉 0.05）. Light microscopy showed that cloud swelling in the cardiac muscle cells and telangicctasia among muscle bundle were seen in the operation control group, and the pathological changes were relatively mild in the edaravone treatment group. Electron microscopy showed mild edema in tunica and focal loosening and disarrangement of myofilament in the operation control group and milder changes in the edaravone group. Conclusion Increasing the SOD activity in blood and the myocardium and decreasing the XOD activity in myocardium, thus enhancing the antioxidating ability and ability to scavenge free radical, edaravone has the function to protect myocardium against the harm of sepsis.