Jurmann M J, Dammenhayn L, Schaefers H J, Haverich A
Department of Thoracic and Cardiovascular Surgery, Hannover Medical School, FRG.
Eur J Cardiothorac Surg. 1990;4(12):665-70. doi: 10.1016/1010-7940(90)90059-9.
Blood granulocyte-mediated reactions involving generation of oxygen-derived free radicals have recently been shown to be capable of causing injury to the lungs. These findings suggest a similar mechanism also to be involved in the development of pulmonary ischemia/reperfusion injury. In the present study, therefore, the effects of three oxygen-derived free radical scavengers, superoxide dismutase (SOD; 1 mg/kg), catalase (20,000 IU/kg) and allopurinol (45 mg/kg), were evaluated during reperfusion in a rabbit model after 2 h normothermic ischemia of the lung. During reperfusion, ischemic lungs were found to have an elevated pulmonary vascular resistance, increased total and extravascular lung water content, and decreased arterial oxygen tension (PaO2) compared to control animals. SOD and catalase, but not allopurinol, were able to reduce pulmonary injury by lowering the pulmonary vascular resistance, but could not prevent pulmonary damage as shown by total lung water (TLW) or PaO2. It is concluded that oxygen-derived free radicals such as hydrogen peroxide and the superoxide anion may play an important role in precipitating pulmonary injury after ischemia. The failure of xanthine oxidase inhibition (allopurinol) to exert protective effects may suggest that oxygen-derived free radical generation following pulmonary ischemia occurs predominantly via leukocyte-mediated reactions.
近期研究表明，血液中粒细胞介导的反应涉及氧衍生自由基的产生，这种反应能够对肺部造成损伤。这些发现提示，类似的机制也可能参与了肺缺血/再灌注损伤的发生发展过程。因此，在本研究中，我们评估了三种氧衍生自由基清除剂，即超氧化物歧化酶（SOD；1毫克/千克）、过氧化氢酶（20,000国际单位/千克）和别嘌呤醇（45毫克/千克），在兔肺常温缺血2小时后再灌注过程中的作用。在再灌注期间，与对照动物相比，发现缺血肺的肺血管阻力升高、肺总含水量和血管外肺含水量增加，动脉血氧分压（PaO2）降低。SOD和过氧化氢酶能够通过降低肺血管阻力减轻肺损伤，但无法像肺总含水量（TLW）或PaO2所显示的那样预防肺损伤。研究得出结论，过氧化氢和超氧阴离子等氧衍生自由基可能在缺血后引发肺损伤中起重要作用。黄嘌呤氧化酶抑制（别嘌呤醇）未能发挥保护作用，这可能表明肺缺血后氧衍生自由基的产生主要通过白细胞介导的反应发生。
