BACKGROUND: In this pilot study, we aimed to investigate the effect of dexmedetomidine on liver tissues during experimental sepsis by histopathological examination. METHODS: The animals were allocated randomly to four groups, two of which received endotoxin. In the Sepsis Group (n:10) and Dexmedetomidine/Sepsis Group (n:10), endotoxemia was induced by E. coli lipopolysaccharide derived from E. coli 0111: B4. Animals in the Control Group (n:10) received an infusion of 0.9% saline (1.0 mL x kg(-1) x hr(-1)) intravenously. The Dexmedetomidine Group (n:10) and Dexmedetomidine/Sepsis Group received a bolus injection of 0.9% saline (1.0 mL/kg), followed by dexmedetomidine administration (infusion at 5 microg x kg(-1) x hr(-1)). All rats were euthanized at the 8th hour of endotoxin infusion. Histopathological examinations were performed on liver tissues. RESULTS: In the liver, central venous congestion, congestion and dilation of the hepatic sinusoids and inflammation of the portal tracts were noted in the Sepsis Group. These parameters were seen slightly in the Sepsis/Dexmedetomidine group. There was a statistically significant difference between the Sepsis and Sepsis/Dexmedetomidine Groups (p<0.001). CONCLUSION: Dexmedetomidine has a protective effect on liver tissues during experimental sepsis in the rat. We propose that dexmedetomidine sedation may be useful in the therapy of the liver dysfunction associated with sepsis and in other diseases related to local or systemic inflammation.
BACKGROUND: In this pilot study, we aimed to investigate the effect of dexmedetomidine on liver tissues during experimental sepsis by histopathological examination. METHODS: The animals were allocated randomly to four groups, two of which received endotoxin. In the Sepsis Group (n:10) and Dexmedetomidine/Sepsis Group (n:10), endotoxemia was induced by E. coli lipopolysaccharide derived from E. coli 0111: B4. Animals in the Control Group (n:10) received an infusion of 0.9% saline (1.0 mL x kg(-1) x hr(-1)) intravenously. The Dexmedetomidine Group (n:10) and Dexmedetomidine/Sepsis Group received a bolus injection of 0.9% saline (1.0 mL/kg), followed by dexmedetomidine administration (infusion at 5 microg x kg(-1) x hr(-1)). All rats were euthanized at the 8th hour of endotoxin infusion. Histopathological examinations were performed on liver tissues. RESULTS: In the liver, central venous congestion, congestion and dilation of the hepatic sinusoids and inflammation of the portal tracts were noted in the Sepsis Group. These parameters were seen slightly in the Sepsis/Dexmedetomidine group. There was a statistically significant difference between the Sepsis and Sepsis/Dexmedetomidine Groups (p<0.001). CONCLUSION:Dexmedetomidine has a protective effect on liver tissues during experimental sepsis in the rat. We propose that dexmedetomidine sedation may be useful in the therapy of the liver dysfunction associated with sepsis and in other diseases related to local or systemic inflammation.