Lung ischemia-reperfusion injury: a molecular and clinical view on a complex pathophysiological process

被引:351
作者
den Hengst, Willem A. [2 ]
Gielis, Jan F. [2 ]
Lin, Judy Y. [1 ]
Van Schil, Paul E. [2 ]
De Windt, Leon J. [1 ]
Moens, An L. [1 ]
机构
[1] Maastricht Univ Med Ctr, Dept Cardiol, Cardiovasc Res Inst Maastricht, NL-6202 AZ Maastricht, Netherlands
[2] Univ Antwerp, Dept Thorax & Vasc Surg, B-2020 Antwerp, Belgium
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2010年 / 299卷 / 05期
关键词
pulmonary; lung transplantation; ventilated ischemia; NITRIC-OXIDE SYNTHASE; TUMOR-NECROSIS-FACTOR; PLATELET-ACTIVATING-FACTOR; CYTOCHROME-C RELEASE; ISOLATED RAT LUNG; ENDOTHELIN RECEPTOR ANTAGONIST; INHALED CARBON-MONOXIDE; EURO-COLLINS SOLUTION; NO-REFLOW PHENOMENON; FACTOR-KAPPA-B;
D O I
10.1152/ajpheart.00251.2010
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
den Hengst WA, Gielis JF, Lin JY, Van Schil PE, De Windt LJ, Moens AL. Lung ischemia-reperfusion injury: a molecular and clinical view on a complex pathophysiological process. Am J Physiol Heart Circ Physiol 299: H1283-H1299, 2010. First published September 10, 2010; doi:10.1152/ajpheart.00251.2010.-Lung ischemia-reperfusion injury remains one of the major complications after cardiac bypass surgery and lung transplantation. Due to its dual blood supply system and the availability of oxygen from alveolar ventilation, the pathogenetic mechanisms of ischemia-reperfusion injury in the lungs are more complicated than in other organs, where loss of blood flow automatically leads to hypoxia. In this review, an extensive overview is given of the molecular and cellular mechanisms that are involved in the pathogenesis of lung ischemia-reperfusion injury and the possible therapeutic strategies to reduce or prevent it. In addition, the roles of neutrophils, alveolar macrophages, cytokines, and chemokines, as well as the alterations in the cell-death related pathways, are described in detail.
引用
收藏
页码:H1283 / H1299
页数:17
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