Punch J, Rees R, Cashmer B, Oldham K, Wilkins E, Smith D J
Department of Surgery, University of Michigan Medical School, Ann Arbor 48109-0340.
J Trauma. 1991 Jun;31(6):760-5; discussion 765-7. doi: 10.1097/00005373-199106000-00005.
In this study, we proposed that oxygen free radicals participate in the acute pulmonary injury that follows limb ischemia/reperfusion. Using an established model of hind limb ischemia, reproducible lung injury occurred after reperfusion. Lung microvascular permeability was measured with 125I-BSA and increased two-fold after 30 minutes of reperfusion. Pulmonary injury was blocked with DMSO, DMTU, allopurinol, indomethacin, and SOD plus catalase. The degree of pulmonary neutrophil sequestration as assessed by tissue myeloperoxidase activity was significantly diminished in animals pretreated with antioxidants. Pretreatment with indomethacin did not attenuate the neutrophil sequestration within the pulmonary parenchyma. These data suggest that increased lung microvascular permeability and neutrophil accumulation occur following hind limb ischemia/reperfusion. Therapeutic interventions with oxygen radical inhibitors blocked this process, while the prostaglandin inhibitor, indomethacin, only reduced lung permeability.
在本研究中，我们提出氧自由基参与肢体缺血/再灌注后的急性肺损伤。使用已建立的后肢缺血模型，再灌注后出现了可重现的肺损伤。用125I-牛血清白蛋白测量肺微血管通透性，再灌注30分钟后增加了两倍。二甲基亚砜、二甲基硫脲、别嘌呤醇、吲哚美辛以及超氧化物歧化酶加过氧化氢酶可阻止肺损伤。通过组织髓过氧化物酶活性评估的肺中性粒细胞滞留程度在经抗氧化剂预处理的动物中显著降低。用吲哚美辛预处理并未减弱肺实质内的中性粒细胞滞留。这些数据表明，后肢缺血/再灌注后肺微血管通透性增加和中性粒细胞积聚。用氧自由基抑制剂进行治疗性干预可阻断这一过程，而前列腺素抑制剂吲哚美辛仅降低肺通透性。
