BACKGROUND: We aimed to demonstrate the time dependent ultrastructural changes in tracheobronchial epithelia after traumatic brain injury. And also, protective effect of erythropoietin was demonstrated. METHODS: We used 56 Wistar-Albino female rats weighing 170 to 200 g. The rats were allocated into 7 groups. First group was the control. The second underwent craniotomy without trauma. The third, fourth, and fifth groups were respectively 2-, 8-, and 24-hour trauma groups. The sixth and seventh groups were respectively treatment (erythropoietin, 1,000 IU/kg) and vehicle (0, 4 ml/rat) groups. Weight-drop method was used for achieving head trauma. Samples were obtained from both trachea and main bronchi. Modified electron microscopic scoring model was used to reveal the ultrastructural changes in both trauma and treatment groups. RESULTS: There was no statistical difference between control and sham groups (p >0.05). Scores of all trauma groups were significantly different from the controls (p <0.05). Trauma produced obvious gradual damage on ultrastructure of the tracheobronchial epithelia. Erythropoietin decreased tracheobronchial scores after traumatic brain injury in significant levels. Erythropoietin attenuated ultrastructural scores for each organelle in significant levels (p <0.05 for each organelle). CONCLUSIONS: The data suggested that ultrastructural damage is obvious at 2 hours deteriorating with time. Erythropoietin protects epithelia against damage after traumatic brain injury. Pharmaceutical lung preservation may help gaining efficacious donor lungs in brain death. But, further time dependent experiments are needed to determine the liability of the donor lung after traumatic brain injury. This fact is to be known for achieving higher graft survival rates.
BACKGROUND: We aimed to demonstrate the time dependent ultrastructural changes in tracheobronchial epithelia after traumatic brain injury. And also, protective effect of erythropoietin was demonstrated. METHODS: We used 56 Wistar-Albino female rats weighing 170 to 200 g. The rats were allocated into 7 groups. First group was the control. The second underwent craniotomy without trauma. The third, fourth, and fifth groups were respectively 2-, 8-, and 24-hour trauma groups. The sixth and seventh groups were respectively treatment (erythropoietin, 1,000 IU/kg) and vehicle (0, 4 ml/rat) groups. Weight-drop method was used for achieving head trauma. Samples were obtained from both trachea and main bronchi. Modified electron microscopic scoring model was used to reveal the ultrastructural changes in both trauma and treatment groups. RESULTS: There was no statistical difference between control and sham groups (p >0.05). Scores of all trauma groups were significantly different from the controls (p <0.05). Trauma produced obvious gradual damage on ultrastructure of the tracheobronchial epithelia. Erythropoietin decreased tracheobronchial scores after traumatic brain injury in significant levels. Erythropoietin attenuated ultrastructural scores for each organelle in significant levels (p <0.05 for each organelle). CONCLUSIONS: The data suggested that ultrastructural damage is obvious at 2 hours deteriorating with time. Erythropoietin protects epithelia against damage after traumatic brain injury. Pharmaceutical lung preservation may help gaining efficacious donor lungs in brain death. But, further time dependent experiments are needed to determine the liability of the donor lung after traumatic brain injury. This fact is to be known for achieving higher graft survival rates.