To observe the expression of calcium/calmodulin dependent protein kinaseⅡ(CaMKⅡ) in the spinal cord of the rats followed lidocaine hydrochloride intrathecal injection.

48 male SD rats weight(230±20)g, after intrathecal indwelling catheter, were randomly divided into four groups (n=12, 8 rats for behavioral detection and 4 rats for western blotting): normal group (C group), sham group (S group), DMSO group (D group), 10% lidocaine group (L group). Mechanical withdrawal threshold(MWT)and thermal withdrawal latency(TWL) were detected before and after 2 h, 4 h, 8 h, 12 h, 1 d, 2 d, 3 d , 4 d and 5 d with drug treatment. Intumescentia lumbalis of the spinal cord were collected to measure the expression of CaMKⅡwith western blotting after drug treatment for 12 h.

The based MWT of the rats in C, S and D group were (11.2±3.1)g, (11.8±2.2)g and (11.4±2.4)g respectively. There were no differences among the every time points (n=8, P>0.05). The MWT of the rats in L group significantly increased at 2 h, 4 h, 8 h, 12 h, 1 d , 2 d, 3 d and 4 d after treatment with lidocaine hydrochloride, and the data were (22.0±6.6)g, (22.2±5.3)g, (20.5±5.8)g, (18.5±4.3)g, (16.7±3.2)g, (15.2±3.1)g, (15.5±3.5)g , (13.7±2.4)g respectively(n=8, P<0.01). TWL had no difference among the rats in C, S, and D group(n=8, P>0.05). The TWL of the rats in L group significantly increased at 2 h, 4 h, 8 h, 12 h, 1 d, 2 d and 3 d after treatment with lidocaine hydrochloride(n=8, P<0.01). The expression of CaMKⅡ of the rats in C group, S group, D group and L group were 0.17±0.03, 0.16±0.03, 0.19±0.05, 0.42±0.11, and significantly upregulated in L goup (n=4, P<0.01).

Lidocaine hydrochloride intrathecal injection can increase the expression of the CaMKⅡin the spinal cord of the rats.Those indicate that CaMKⅡ may be involved with the nerve damage induced by lidocaine hydrochloride.

Lidocaine hydrochloride; Spinal cord; Nerve damage; Calcium/calmodulin dependent protein kinaseⅡ