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小鼠感染旋毛虫后心肌ＸＯＤ及ＭＤＡ随感染时间的延长逐渐升高，二者分别从第７ｄ和第１４ｄ起含量明显高于正常组（ｔ＜０．０５～０．０１），血清ＭＤＡ于感染后第１４ｄ最高（ｐ〈０．０１）到第３０ｄ稍有回降。表明：小鼠感染旋毛虫后心肌自由基产生随进入心肌旋毛虫毒素的增加或进入人心肌幼虫的增多而增加，可能是导致旋毛虫性心肌病变的主要原因。小鼠心肌ＧＳＨ除第３０ｄ明显高于正常组，余者升高不明显；血清ＧＳＨ于感染后３ｄ明显升高，第７、１４ｄ尤其是第３０ｄ较前者有所回降（但仍高于正常组）。我们推测小鼠感染旋毛虫后组织及血清中ＧＳＨ可能主要来自于虫体，即旋毛虫抵抗宿主感染期间释放自由基时可以产生ＧＳＨ。这一结果将为进一步了旋毛虫性心肌炎的致病机理及虫体逃避宿主效应与提高宿主抗旋毛虫的感染机制提供资料。
The XOD and MDA of the mice infected with Trichinella increased gradually with the prolongation of infection time. The contents of XOD and MDA in the mice infected with Trichinella spiralis were significantly higher than those in the normal control group from the 7th day and the 14th day respectively (t <0.05 ~ 0.01) The highest 14th day after infection (p <0.01) and a slight fall back to the 30th day. The results showed that the generation of free radicals in myocardium of mice infected with Trichinella increased with the increase of enteritidistris toxin or the influx into human myocardial larvae, which may be the main cause of Trichinella causing cardiomyopathy. GSH in myocardium of mice was significantly higher than that of the normal group on the 30th day, while the others did not increase obviously. Serum GSH increased significantly on the 3rd day after infection, but decreased on the 7th, 14th, especially 30th group). We speculated that mice infected with Trichinella tissue and serum GSH may be mainly from the parasites, that is, Trichinella resistant to host infection during the release of free radicals can produce GSH. This result will provide further information on the pathogenesis of Trichinella spiralis myocarditis and its effect of avoiding the host and increasing the host anti-Trichinella infection mechanism.