Onur Karaca1, Güvenç Doğan2. 1. Department of Anesthesiology and Reanimation, Aksaray University Faculty of Medicine, Aksaray-Turkey. 2. Department of Anesthesiology and Reanimation, Hitit University Faculty of Medicine, Çorum-Turkey.
Abstract
BACKGROUND: This study aims to investigate whether or not dexmedetomidine (DEX) application affects inflammation, increased intestinal mucosa damage and intestinal permeability in traumatic brain injury (TBI). METHODS: The rats included in our study were randomized into three groups as the control group (Group 1, n=10), trauma group (Group 2, n=10) and the trauma+dexmedetomidine group (Group 3, n=10). While trauma was not induced in the control group, head trauma was induced in all rats in Groups 2 and 3 with the same method. The rats in Group 3 additionally received the DEX application. Intestinal THF-a, serum TNF-a, IL-6, IL-1b and D-lactate levels were measured six hours post-trauma to assess systemic and local infection. Histopathological evaluation of the terminal ileum was performed at the 6th hour to assess mucosal damage. Intestinal permeability was evaluated by measuring the level of dextran injected into the 5-cm ileum segment adhered to the proximal and distal edges at the 30th minute in the blood taken by cardiac puncture. RESULTS: Intestinal TNF-a (p=0.003), serum TNF-a (p=0.009), IL-6 (p=0.002), IL-1b (p=0.001), and D-lactate levels measured in Group 3 (p=0.046) were significantly lower than those measured in Group 2. Dextran level measured in blood in Group 3 was observed significantly lower than that of Group 2 (p<0.001). Histopathological evaluation of the intestines revealed no injuries in the ileum of the rats in Group 1, injury in the ileum, villus atrophy and mucosal damage in the rats in Group 2, and a significant recovery was observed in Group 3 in comparison to Group 2. CONCLUSION: It was seen in our study that DEX reduced TBI-induced increased inflammation, intestinal mucosa damage and intestinal permeability. These results suggest that DEX may ameliorate the damage done to the intestinal tissue by modulating post-TBI inflammatory responses.
BACKGROUND: This study aims to investigate whether or not dexmedetomidine (DEX) application affects inflammation, increased intestinal mucosa damage and intestinal permeability in traumatic brain injury (TBI). METHODS: The rats included in our study were randomized into three groups as the control group (Group 1, n=10), trauma group (Group 2, n=10) and the trauma+dexmedetomidine group (Group 3, n=10). While trauma was not induced in the control group, head trauma was induced in all rats in Groups 2 and 3 with the same method. The rats in Group 3 additionally received the DEX application. Intestinal THF-a, serum TNF-a, IL-6, IL-1b and D-lactate levels were measured six hours post-trauma to assess systemic and local infection. Histopathological evaluation of the terminal ileum was performed at the 6th hour to assess mucosal damage. Intestinal permeability was evaluated by measuring the level of dextran injected into the 5-cm ileum segment adhered to the proximal and distal edges at the 30th minute in the blood taken by cardiac puncture. RESULTS: Intestinal TNF-a (p=0.003), serum TNF-a (p=0.009), IL-6 (p=0.002), IL-1b (p=0.001), and D-lactate levels measured in Group 3 (p=0.046) were significantly lower than those measured in Group 2. Dextran level measured in blood in Group 3 was observed significantly lower than that of Group 2 (p<0.001). Histopathological evaluation of the intestines revealed no injuries in the ileum of the rats in Group 1, injury in the ileum, villus atrophy and mucosal damage in the rats in Group 2, and a significant recovery was observed in Group 3 in comparison to Group 2. CONCLUSION: It was seen in our study that DEX reduced TBI-induced increased inflammation, intestinal mucosa damage and intestinal permeability. These results suggest that DEX may ameliorate the damage done to the intestinal tissue by modulating post-TBI inflammatory responses.