RESUMO
BACKGROUND: Sepsis is one of the leading causes of death in intensive care units. Dexmedetomidine is a sedative agent with anti-inflammatory properties. This study is designed to differentiate the impact of two different doses of dexmedetomidine on lung injury induced by sepsis. METHODS: Adult male Wistar rats were randomly divided into four groups: sham (nâ¯=â¯6), control (nâ¯=â¯12), 5DEX (nâ¯=â¯12), and 10DEX (nâ¯=â¯12). Cecal ligation puncture (CLP) was applied for sepsis initiation. The 5DEX group received 5⯵g.kg-1.h-1 and the 10DEX group received 10⯵g.kg-1.h-1 dexmedetomidine intravenous infusions for a 1-hour period. Six hours after CLP, tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and intercellular adhesion molecule-1 (ICAM-1) levels were analyzed in blood samples. Twenty-four hours after CLP, lung samples from the remaining rats were collected for the measurement of myeloperoxidase (MPO) activity, histological examination, and TdT- (terminal deoxynucleotidyl transferase) mediated fluorescent-dUTP labeling staining for apoptosis detection. RESULTS: Serum cytokine release, MPO activity, and apoptosis in the lung were significantly increased in the CLP group compared with the sham and dexmedetomidine groups (pâ¯<â¯0.05). TNF-α, ICAM-1, and MPO were significantly lower in the 10DEX group compared with both 5DEX and control groups, while IL-1ß, total injury score, and apoptotic cell count had significantly lower values in both 10DEX and 5DEX groups compared with the control group (pâ¯<â¯0.05). CONCLUSION: Dexmedetomidine administration played a protective role against CLP-induced lung injury. High-dose dexmedetomidine was needed for suppressing the leukocyte-mediated lung injury and apoptosis of lung tissue.