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Donation after brain death has been the main source for organ transplantation. It is important to develop an effective method to protect the organ and improve its quality.


To investigate the effect of heat shock protein 70 on rabbit brain death induced lung injury.


The 60 rabbits were randomly divided into three groups: rabbits in the normal control group without surgery; the rabbits in the sham-operation group received femoral artery catheterization, endotracheal intubation and burr hole catheter, did not received the intracranial pressure; and the rabbits in the brain death group were treated with femoral artery catheterization, endotracheal intubation, burr hole catheter and intracranial pressure, and the ventilator was used to maintain a brain-dead state. Each group was further divided into four time points at 2, 4, 6 and 8 hours. The blood pressure and the heart rate were measured at each point. The changes of lung morphology were observed by hematoxylin-eosin staining. The mRNA and the protein expression of heat shock protein 70 were measured by reverse transcription-PCR and immunohistochemistry.


There was no significant difference in the blood pressure and the heart rate between the brain death group and sham-operation group (P > 0.05). The lung injuries in the sham-operation group at different time points were not obvious. From 2 to 6 hours, the lung injuries in the brain-death groups were getting worse in a time-dependent manner (P < 0.05), but somewhat amelioration at 8 hours group was observed when compared with the previous time group. The mRNA and the protein expression of heat shock protein 70 were gradually increased at 2 hours in a time-dependent manner (P < 0.05) and reached peak at 8 hours. These findings confirm that heat shock protein 70 can ameliorate brain death induced lung injury and play their defensive protection effect.

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