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.OBJECTIVE:
To investigate the effect of heat shock protein 70 on rabbit brain death induced lung injury.METHODS:
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.RESULTS AND CONCLUSION:
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.