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对８１例急性心肌梗塞患者行尿激酶１００～１５０万Ｕ静脉溶栓治疗，再通１８例，未通１３例。再通组其溶栓治疗后４、１２、２４和７２小时测定的血浆丙二醛（ＭＤＡ）浓度较溶栓前显著升高（Ｐ＜０．０１），同期测定的血尿酸（ＵＡ）浓度在溶栓治疗后４小时较溶栓前明显升高（Ｐ＜０．０５），未通组的血浆ＭＤＡ和ＵＡ浓度在溶栓前后均无明显变化（Ｐ＞０．０５）。溶栓治疗后４小时血浆ＭＤＡ和ＵＡ浓度的变化，在再通组呈正相关（ｒ＝０．４３，Ｐ＜０．０１），未通组则无相关关系（ｒ＝０．０２７，Ｐ＞０．０５）。说明人体缺血心肌再灌注时有氧自由基（ＯＦＲ）生成。黄嘌呤氧化酶系统是人体ＯＦＲ生成的主要途径。
81 cases of acute myocardial infarction patients with urokinase 100 ~ 1500000 U intravenous thrombolytic therapy, and then in 18 cases, failed in 13 cases. The levels of plasma malondialdehyde (MDA) measured at 4, 12, 24 and 72 hours after thrombolytic therapy in thrombolytic therapy group were significantly higher than those before thrombolytic therapy (P <0.01). The serum uric acid (UA) Thrombolytic therapy at 4 hours after thrombolysis was significantly higher (P <0.05), the non-pass group plasma MDA and UA concentrations before and after thrombolysis did not change significantly (P> 0.05). Plasma concentrations of MDA and UA at 4 hours after thrombolytic therapy showed no significant correlation with recanalization (r = 0.43, P <0.01) and no correlation (r = 0.027, P> 0.05). Description of human ischemia myocardial reoxygenation free radical (OFR) generation. Xanthine oxidase system is the main way of human OFR generation.