Lung injury and inflammatory responses in a rabbit model of brain death

BACKGROUND: The quality of organs from donation after brain death is essential for the success of transplantation. Studies on the mechanism and protection of organ injury induced by brain death will provide references for the reasonable application of donor organs. OBJECTIVE: To investigate the changes in the liver morphology and inflammatory factors at different time points after brain death in rabbits, and to explore the mechanism of inflammatory factors in lung damage induced by brain death. METHODS: Forty rabbits were randomized into two groups (n=20 per group): Sham operation group (tracheal intubation, femoral artery intubation, and sphenotresia), brain death group (low intracranial pressure to establish a state of brain death). The mean arterial pressure and heart rate in the two groups were recorded at postoperative 2, 6, 8 hours; the pathological changes of lung were observed by hematoxylin-eosin staining. The expression levels of inflammatory factors in the lung tissues including heat shock protein 27, intercellular adhesion molecule-1 and nuclear factor-KB were tested by RT-PCR and immunohistochemistry. The serum levels of interleukin-1, -6, and -8 were detected by ELISA. RESULTS AND CONCLUSION: There were no significant differences in the mean arterial pressure and heart rate at 2, 6 and 8 hours after brain death (P>0.05). The serum levels of interleukin-1, -6, and -8 increased with time, and the differences were significant (P<0.05). The mRNA level of heat shock protein 27 in the brain death group was significantly higher than that in the sham operation group (P<0.05). Under light microscope, the alveolar cavity was intact at 2 hours after brain death, capillary hemorrhage, widened alveolar septum and inflammatory cell infiltration occurred at 6 hours after brain death, and inflammatory cells almost infiltrated the entire lung at 8 hours, which were consistent with the expression levels of inflammatory factors like intercellular adhesion molecule-1 and nuclear factor-KB in the brain death group. In summary, brain death can lead to lung damage, which gets worse with time, and the damage is related to the release of inflammatory factors. Moreover, the lung damage peaks at 8 hours after brain death.