Effect of dexmedetomidine on activations of pulmonary ERK 1/2 and Akt during isolated lung ischemia-reperfusion injury in rats / 临床麻醉学杂志

ABSTRACT

Objective To investigate the effect of dexmedetomidine on activations of pulmonary extracellular signal-regulated kinase 1/2 (ERK 1/2 )and serine-threonine kinase (Akt) during isolated lung ischemia-reperfusion injury (LIRI)in rats.Methods Forty-five adult male Spra-gue-Dawley rats were randomly divided into three groups (n=1 5 each)control group (group C),is-chemia-reperfusion group (group IR)and dexmedetomidine group (group DEX).Isolated rat lungs were maintained for normal physical activity,and only received ventilation and perfusion for 150 min in the IL-2 ex-vivo lung perfusion system in group C.Isolated rat lungs were subjected to 60 min of is-chemia and apnea followed by 75 min reperfusion and ventilation 15 min after perfusion in the IL-2 ex-vivo lung perfusion system in groups IR and DEX.Dexmedetomidine with a dose of 10 nmol/L was ad-ministrated into perfusion fluid at the onset of reperfusion in group DEX,and the same volume of saline was injected when perfusion for 75 min and at the onset of reperfusion in groups C and IR,respectively.Patho-logical changes of lungs were examined and the injured alveolus rate (IAR)was counted under light micro-scope.The expression levels of ERK 1/2 or Akt mRNA and phosphorylate-ERK 1/2 (p-ERK 1/2 )or phosphorylate-Akt (p-Akt)protein of lung tissue were tested by reverse transcription-polymerase chain re-action (RT-PCR)and Western blot,respectively.Results Compared with group C,the IAR and the ex-pression levels of ERK 1/2 and Akt mRNA or p-ERK 1/2 and p-Akt protein in lung tissue were high-er in groups IR and DEX (P<0.05).Compared with group IR,the IAR and the expression levels of ERK 1/2 and Akt mRNA or p-ERK 1/2 and p-Akt protein in lung tissue were lower in group DEX (P<0.05).Conclusion Dexmedetomidine may reduce LIRI in rat isolated lungs via inhibiting the expressions of IL-6 and IL-8,and the mechanism may be related to suppressing activations of ERK 1/2 and Akt.