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单甲氧基聚乙二醇（ＭＰＥＧ）活化后与超氧化物歧化酶（ＳＯＤ）偶联，经纯化后得到ＭＰＥＧ－ＳＯＤ，鉴定其分子量约为７．０×１０５Ｄａｔｉｏｎ。其在血液循环中酶活性半衰期超过３０ｈ，远大于天然ＳＯＤ（６－１０ｍｉｎ）。ＳＤ雄性大鼠分三组．对照组（ｎ＝８．由股静脉注入０．２ｍｌ生理盐水）、ＮａｔｉｖｅＳＯＤ组（ｎ＝８，注以０．２ｍｌ生理盐水配的８００ＵＳＯＤ）和ＭＰＥＧ－ＳＯＤ组（ｎ＝９，注以８００ＵＭＰＥＧ－ＳＯＤ）。低氧前三组鼠的心率（ＨＲ）、左室内峰压（ＬＶＰ）、左室压微分（ＬＶ±ｄｐ／ｄｔｍａｘ）和股动脉压（ＡＰ）均无统计学差别。在模拟６０００—６５００ｍ高度急性低氧１．８．１４ｍｉｎ记录上述各项指标，结果如下：除ＨＲ外，ＮａｔｉｖｅＳＯＤ组与对照组各指标均无统计学差别，ＭＰＥＧ－ＳＯＤ组的各项指标均明显高于对照组。表明ＭＰＥＧ－ＳＯＤ对急性低氧导致的左心室力学指标的减弱有明显保护作用，提示超氧自由基（Ｏ２－）在急性低氧导致左心室功能损伤中起重要作用，即可能是由Ｏ２－及其衍生的其它自由基损害心肌细胞生物膜系统所致。
After the activation of monomethoxypolyethylene glycol (MPEG), it was coupled with superoxide dismutase (SOD). After purification, MPEG-SOD was obtained and its molecular weight was estimated to be about 7.0 × 105Dation. Its half-life of enzymatic activity in the blood circulation more than 30h, much larger than the natural SOD (6-10min). SD male rats were divided into three groups. The rats in the control group (n = 8, 0.2 ml normal saline injected into femoral vein), NativeSOD group (n = 8, 800USD injected with 0.2 ml saline) and MPEG-SOD group SOD). There was no significant difference in heart rate (HR), left ventricular peak pressure (LVP), LV ± dp / dtmax and femoral artery pressure (AP) between the three groups before hypoxia. The above indicators were recorded in a simulated acute hypoxia 6000-6500m 1.8.14min, the results are as follows: In addition to HR, there was no significant difference between the indicators of the NativeSOD group and the control group, the indicators of the MPEG-SOD group were significantly Higher than the control group. These results indicate that MPEG-SOD has a significant protective effect on the decrease of left ventricular mechanical parameters induced by acute hypoxia, suggesting that superoxide radical (O2-) plays an important role in the pathogenesis of acute hypoxia-induced left ventricular dysfunction, which may be caused by O2- And other derived free radicals damage cardiomyocyte biofilm system.