Objective To evaluate the changes in the expression of spinal aquaporin-4 (AQP4) during remifentanil-induced hyperalgesia in a mouse model of incisional pain.Methods Seventy-two pathogen-free healthy adult male CD1 mice,weighing 25-30 g,were divided into 4 groups (n=18 each) using a random number table:control group (group C),incisional pain (group I),remifentanil group (group R) and remifentanil plus incisional pain group (group R+I).Normal saline was infused subcutaneously in group C.An incision was made in the left hind paw in group I.Remifentanil 80 μg/kg was subcutaneously infused for 30 min at a rate of 0.8 ml/h in group R.Remifentanil was infused subcutaneously before establishment of the model in group R+I.The thermal paw withdrawal latency (TWL) and mechanical paw withdrawal threshold (MWT) were measured at 1 day before establishment of the model (T0) and 6 h and 1,2 and 7 days after establishment of the model (T1-4).After measurement of the pain threshold at T3,12 animals were sacrificed randomly,and the lumbar segment of the spinal cord was removed for determination of the distribution and expression of AQP4 by Western blot.Results Compared with group C,the TWL was significantly shortened at T1-3,and the MWT was decreased at T2-4 in R and R + I groups,and the expression of AQP4 was significantly up-regulated at T3 in I,R and R+I groups (P＜0.05).Compared with group I,the TWL was significantly shortened at T2,3,and the MWT was decreased at T2.4 in group R,and the TWL was significantly shortened at T1-3,the MWT was decreased at T2.4,and the expression of AQP4 was up-regulated at T3 in group R+I (P＜0.05).Conclusion The mechanism by which remifentanil induces hyperalgesia is related to up-regulation of AQP4 expression in the spinal cord in a mouse model of incisional pain.

Objective To evaluate the effects of remifentanil post-conditioning on aquaporin-1 (AQP-1) expression during myocardial ischemia-reperfusion (I/R) injury in rats.Methods Twenty-four male.SpragueDawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =8 each) using a random number table:sham operation group (group S),group I/R,and remifentanil post-conditioning group (group RP).Myocardial I/R was induced by 45 min occlusion of left anterior descending branch of coronary artery followed by 24 h reperfusion.Remifentanil 10 μg· kg-1· min-1 was infused over 10 min starting from 10 min before reperfusion in group RP,while the equal volume of normal saline was given instead in S and I/R groups.At the end of reperfusion,all the rats were sacrificed and their myocardial specimens from left ventricles were obtained for microscopic examination of thepathological changes and for determination of AQP-1 mRNA (using real-time fluorescent quantitative PC R) and AQP-1 protein (by Western blot) expression in the ischemic area and myocardial water content.Results Compared with S group,myocardial water content was significantly increased in the other two groups,AQP-1 mRNA and protein expression was up-regulated in group I/R,and no significant change was found in AQP-1 mRNA and protein expression in RP group.Compared with I/R group,myocardial water content was significantly reduced,and AQP-1 mRNA and protein expression was down-regulated in RP group.Conclusion Remifentanil post-conditioning reduces myocardial I/R injury possibly through down-regulating AQP-1 expression in myocardial tissues of rats.