Brown J M, Terada L S, Grosso M A, Whitman G J, Velasco S E, Patt A, Harken A H, Repine J E
Department of Surgery, University of Colorado Health Sciences Center, Denver.
Mol Cell Biochem. 1988 Dec;84(2):173-5. doi: 10.1007/BF00421052.
In an isolated, normothermic rat heart model (Langendorff, 37 degrees C), dimethylthiourea (DMTU) infusion only during reperfusion reduced both injury and measurable hydrogen peroxide (H2O2) concentrations after global ischemia. Cardiac function was assessed by measurement of ventricular developed pressure (DP). H2O2 was assessed using H2O2 dependent aminotriazole inactivation of myocardial catalase. Depletion of xanthine oxidase by two methods (tungsten or allopurinol inhibition) also improved recovery of function and H2O2 production. The results indicate that XO derived H2O2 contributes to myocardial reperfusion injury.
在一个离体、正常体温的大鼠心脏模型（Langendorff，37摄氏度）中，仅在再灌注期间输注二甲基硫脲（DMTU）可降低全心缺血后的损伤以及可测量的过氧化氢（H2O2）浓度。通过测量心室舒张末压（DP）评估心脏功能。使用依赖H2O2的氨基三唑使心肌过氧化氢酶失活来评估H2O2。通过两种方法（钨或别嘌呤醇抑制）消耗黄嘌呤氧化酶也可改善功能恢复和H2O2生成。结果表明，黄嘌呤氧化酶衍生的H2O2促成心肌再灌注损伤。
