Study of dexmedetomidine alleviating propofol infusion syndrome in rats
Objective To investigate the protective mechanism of dexmedetomidine on organ damage in-duced by propofol infusion syndrome in rats.Methods 18 healthy male SD rats,aged 8~10 weeks and weighing 250~280 g were randomly divided into control group(Group C),propofol group(Group P)and dexmedetomidine group(Group D).The rats in each group were infused with saline,propofol and dexme-detomidine+propofol in the tail vein,respectively.In each group,blood serum samples were collected from the carotid artery of the rats at T0,T6,and T12 to measure the levels of ALT,AST,CK,CK-MB,BUN,Cr and cTn-I.Myocardial tissues from the rats were collected after the infusion was completed in each group.The tissues were stained with HE staining to observe the structural changes of the myocardi-um.The activity of mitochondrial respiratory complex Ⅱ,cytochrome C,CPT-I and Maltomide were de-tected in the cardiac muscle tissues using the ELISA method.Results Compared with group C,the levels of ALT,AST,CK,CK-MB,BUN and cTn-I in group P were increased at T6 and T12;The levels of ALT,AST,CK,CK-MB,BUN and Cr were increased at T6 and T12 in group D,and cTn-I was increased at T6 in group D(P<0.05).Compared with group P,the levels of ALT,AST,CK and cTn-I in group D were decreased averagely at T6 and T12,and the levels of CK-MB and BUN were decreased at T12(P<0.05).The results suggested that group P had disordered myocardial fibre arrangement,with cell oedema,lysis and scattered inflammatory cell infiltration.In contrast,group D had a more regular and neat myo-cardial fibre arrangement.Compared with group C,the activity of respiratory chain complex Ⅱ and the ex-pression of Cyt-C,CPT-I and Malonyl-CoA were decreased in group P and D(P<0.05).Compared with group P,the activity of complex Ⅱ and the expression levels of Cyt-C,CPT-I and Malonyl-CoA were in-creased in group D(P<0.05).Conclusion Dexmedetomidine attenuates the organ damage induced by propofol infusion syndrome in rats and the mechanism may be related to attenuation of mitochondrial respiratory chain dysfunction and improvement in fatty acid catabolism.