Haklar G, Erşahin C, Moini H, Süngün M, Doğan N, Bilsel S, Emerk K, Yalçin A S
Department of Biochemistry, Faculty of Medicine, Marmara University, Haydarpaşa-Istanbul, Turkey.
Arzneimittelforschung. 1996 Apr;46(4):381-4.
Ischemia followed by reperfusion has deleterious effects on myocardial tissue and a wide range of drugs have been investigated to modulate these changes. Defibrotide (polydeoxyribonucleotides from bovine lung), a drug with antithrombotic and fibrinolytic activities, has also proven to be cardioprotective against myocardial ischemia/reperfusion damage. However, the mechanism of this protective effect has not been clarified yet. The aim of this study was to determine whether this effect is due to protection against free radical induced changes. The experimental model in rabbits includes coronary artery ligation for 60 min followed by a reperfusion period of 45 min. In this model, free radical damage was estimated by different parameters of lipid peroxidation such as diene conjugation, carbonyl content, and thiobarbituric acid reactive substances, together with protein oxidation determinations. The results demonstrate that defibrotide prevents free radical induced changes after myocardial ischemia/reperfusion.
缺血后再灌注会对心肌组织产生有害影响，人们已经研究了多种药物来调节这些变化。去纤苷（来自牛肺的多脱氧核糖核苷酸）是一种具有抗血栓形成和纤维蛋白溶解活性的药物，已被证明对心肌缺血/再灌注损伤具有心脏保护作用。然而，这种保护作用的机制尚未阐明。本研究的目的是确定这种作用是否归因于对自由基诱导变化的保护。兔实验模型包括冠状动脉结扎60分钟，随后再灌注45分钟。在该模型中，通过脂质过氧化的不同参数（如二烯共轭、羰基含量和硫代巴比妥酸反应性物质）以及蛋白质氧化测定来评估自由基损伤。结果表明，去纤苷可防止心肌缺血/再灌注后自由基诱导的变化。
