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J Thorac Cardiovasc Surg 2008;136:352-359
© 2008 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Comparison between adult and infant lung injury in a rabbit ischemia-reperfusion model

Wanshan Qiu, MDa,b,c, Liang Zheng, MDa, Haiyong Gu, MDa, Duan Chen, MD, PhDc, Yijiang Chen, MDa,*

a Department of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
b Department of Thoracic and Cardiovascular Surgery, The Affiliated Children's Hospital of Nanjing Medical University, Nanjing, China
c Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway

Received for publication October 25, 2007; revisions received January 2, 2008; accepted for publication January 7, 2008.

* Address for reprints: Yijiang Chen, MD, Department of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China. (Email: yjchen{at}NJMU.edu.cn).

Objective: Ischemia-reperfusion causes lung damage to patients with congenital heart disease who undergo open surgery under total cardiopulmonary bypass. The aim of the present study was to compare ischemia-reperfusion–induced lung damage between adults and infants.

Methods: Both infant (15 to 21-day-old) and adult (5 to 6-month-old) rabbits were subjected to either ischemia-reperfusion or sham operation. Ischemia-reperfusion was induced by clamping the right pulmonary hilum for 1 hour and then removing the clamp for 4 hours. The lung tissue samples were collected for histologic examination by light and electron microcopies and for biological evaluation of mitochondrial alterations. Blood samples were taken for measurement of interleukin-1β and tumor necrosis factor-{alpha}. Differences among the groups were analyzed by 2-way analysis of variance.

Results: In comparison with adult lungs, the infant lungs had increased neutrophil infiltration, edema, swollen alveolar epithelial and endothelial cells, and severe mitochondrial impairment reflected by reduced swelling rate and membrane potential, intramitochondrial free Ca2+ levels after ischemia-reperfusion. The infant lungs produced higher levels of hydroxyl radical and malondialdehyde and lower levels of superoxide dismutase and glutathione peroxidase than adult lungs, especially after ischemia-reperfusion. The circulating levels of interleukin-1β and tumor necrosis factor-{alpha} were elevated during ischemia-reperfusion, particularly in the infants, which appeared to be associated with the expression of myeloid differentiation factor-88 and nuclear factor-{kappa}B in the lungs.

Conclusion: Lung ischemia-reperfusion causes more severe lung damage in infants than in adults, probably because of the combination of low antioxidant capacity and overproduction of reactive oxygen species in infants.

Abbreviations and Acronyms GSH-PX = glutathione peroxidase; IL = interleukin; IR = ischemia-reperfusion; MDA = malondialdehyde; MyD = myeloid differentiation factor; NF-{kappa}B = nuclear factor-{kappa}B; ROS = reactive oxygen species; ROS-HR = reactive oxygen species-hydroxyl radical; SOD = superoxide dismutase; TNF = tumor necrosis factor






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