星状神经节阻滞对炎症痛兔血清皮质醇和白介素-8的影响

目的研究星状神经节阻滞(SGB)对福尔马林诱导的兔伤害反应、血清皮质醇(CS)和白介素8(IL8)的影响。方法用手术法在兔星状神经节附近置入导管,选择24只随机分为三组假手术组(A组)、SGB组(B组)和对照组(C组)。B和C组在右前肢足底皮下注射3%福尔马林0.5ml致痛,A组同样部位注射等量生理盐水。致痛前10min,B组经导管注射0.25%布比卡因0.5ml,A和C组注射等量生理盐水。致痛前10min(T0)、致痛后10(T1)、60(T2)和120min(T3)取静脉血,放免法测血清CS和IL8浓度。结果SGB后福尔马林诱导的Ⅱ期伤害反应明显缓解。C组致痛后血清CS浓度显著升高,在T2时点达高峰(P<0.01);B组致痛后血清CS浓度无明显升高(P>0.05),与C组比有显著性差异(P<0.05)。B组和C组T2和T3时点血清IL8浓度较T0及T1时点显著升高(P<0.01);B组T2和T3时点血清IL8浓度明显低于C组同时点(P<0.01)。结论SGB可减轻福尔马林诱导的Ⅱ期伤害反应,可抑制福尔马林刺激引起的血清CS和IL8浓度升高,这些改变可能与其治疗炎症痛机制有关。

EFFECT OF STELLATE GANGLION BLOCK ON SERUM CONCENTRATION OF CORTISOL AND INTERLEUKIN-8 IN RABBITS WITH FORMALIN-INDUCED PAIN

Objective: To investigate formalin induced nociceptive behavior and changes of cortisol(CS) and interleukin 8 (IL 8) in serum following stellate ganglion block (SGB) in rabbits. Methods: Catheters were inserted closely to right stellate ganglia in rabbits.Twenty four rabbits were randomly divided into three groups: group A receiving 0.5ml of normal saline, group B and C receiving as ml of 3% formalin via intraplantar injection into the right front paw, respectively. Ten min before stimulation,0.5 ml of 0.25% bupivacaine was administered via the catheter in group B,while in group A and C 0.5 ml of normal saline was applied. Nociceptive behavior was observed for one hour using weighted pain score.Serum CS and IL 8 were measured radioimmunologically at 10 min(T 0) before stimulation,10(T 1),60(T 2) and 120 min(T 3) after stimulation. Results: Formalin induced nociceptive behavior in phase 2 was relieved following SGB.Serum CS concentration increased significantly after formalin stimulation and reached peak at T 2 in group C ( P <0.01),while it was unchanged in group B. There was significant difference between group B and C. Serum IL 8 concentration in group B and C persistently increased at T 2 and T 3 ( P <0.01), where group B was also significantly lower than group C ( P <0.01). Conclusions: The elevation of serum cortisol and IL 8 concentration was suppressed by SGB.It may be one of the mechanisms of SGB for the treatment of inflammatory pain.