To evaluate the changes in the expression of spinal divalent metal transporter 1 (DMT1) during remifentanil-induced hyperalgesia in a rat model of incisional pain.

Thirty-two male Sprague-Dawley rats, weighing 240-260 g, aged 2-3 months, were randomly divided into 4 groups (n=8 each) using a random number table: control group (group C), incisional pain group (group I), remifentanil group (group R), and incisional pain+ remifentanil group (group I+ R). In group C, normal saline was infused for 60 min at a rate of 0.1 ml·kg^-1·min^-1.A 1-cm longitudinal incision was made through skin, fascia and muscle of the plantar aspect of the left hindpaw in sevoflurane-anesthetized rats, and normal saline was infused intravenously for 60 min at a rate of 1.0 μg·kg^-1·min^-1 at the same time in group I. In group R, remifentanil was infused for 60 min at a rate of 1.0 μg·kg^-1·min^-1.In group I+ R, the model of incisional pain was established, and remifentanil was simultaneously infused for 60 min at a rate of 1.0 μg·kg^-1·min^-1.At 24 h before normal saline or remifentanil infusion and 6, 24 and 48 h after the end of infusion (T_0-3), the mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured.All the rats were sacrificed after the last measurement of pain thresholds, and the spinal cord was removed for determination of DMT1 with/without iron-responsive element [DMT1(+ )IRE and DMT1(-)IRE] expression (by Western blot analysis and immunohistochemistry).

Compared with group C, the MWT was significantly decreased, and the TWL was significantly shortened at T_1-3, and the expression of spinal DMT1(-)IRE was significantly up-regulated in I, R and I+ R groups (P<0.05). Compared with I and R groups, the MWT was significantly decreased, and TWL was significantly shortened at T_1-3, and the expression of spinal DMT1(-)IRE was significantly up-regulated in group I+ R (P<0.05). There was no significant difference in the expression of spinal DMT1(+ )IRE between the four groups (P>0.05).

Spinal DMT1(-)IRE activation may be involved in the mechanism underlying remifentanil-induced hyperalgesia in a rat model of incisional pain.

Piperidines; Pain, postoperative; Hyperalgesia; Cation transport proteins; Spinal cord