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Updated: Jul 2, 2026
Model of Ischemia and Reperfusion Injury in Rabbits
Published on: November 3, 2023
Comparison between adult and infant lung injury in a rabbit ischemia-reperfusion model
Wanshan Qiu1, Liang Zheng, Haiyong Gu
1Department of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Insights
Infant lungs experience more severe ischemia-reperfusion injury than adult lungs, likely due to lower antioxidant capacity and higher reactive oxygen species production. This finding is critical for understanding lung damage in pediatric congenital heart disease surgery.
Area of Science:
- Cardiovascular Surgery
- Pediatric Cardiology
- Pulmonary Medicine
Background:
- Ischemia-reperfusion (I/R) injury is a significant complication in patients with congenital heart disease undergoing cardiopulmonary bypass.
- Understanding age-related differences in lung injury is crucial for optimizing surgical outcomes.
Purpose of the Study:
- To compare the severity of ischemia-reperfusion-induced lung damage between infant and adult rabbits.
- To investigate the underlying mechanisms contributing to potential differences in lung injury.
Main Methods:
- Rabbits of different age groups (infants: 15-21 days; adults: 5-6 months) underwent pulmonary ischemia-reperfusion or sham procedures.
- Histological examination, mitochondrial function assessment, and measurement of inflammatory markers (interleukin-1 beta, tumor necrosis factor-alpha) were performed.
- Analysis included evaluation of reactive oxygen species and antioxidant enzyme levels.
Main Results:
- Infant lungs exhibited increased neutrophil infiltration, edema, and cellular swelling compared to adult lungs post-I/R.
- Mitochondrial impairment was more pronounced in infant lungs, evidenced by reduced swelling rate and membrane potential.
- Infants showed higher levels of hydroxyl radical and malondialdehyde, and lower levels of superoxide dismutase and glutathione peroxidase, alongside elevated inflammatory cytokines.
Conclusions:
- Infants sustain more severe lung ischemia-reperfusion injury than adults.
- Lower antioxidant capacity and increased reactive oxygen species production in infants contribute to heightened lung damage.
- These findings highlight critical age-dependent vulnerabilities in lung response to surgical stress.
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-1 beta 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 Ca(2+) 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-1 beta 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-kappaB 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.
