血管紧张素Ⅱ受体在大鼠神经病理性痛形成中的作用

Role of angiotensin Ⅱ receptors in development of neuropathic pain in rats

目的评价血管紧张素Ⅱ受体在大鼠神经病理性痛形成中的作用。方法健康雄性sD大鼠75只，体重230-270g，采用随机数字表法，将其分为5组（n=15）：假手术组（S组）、神经病理性痛组（NP组）、血管紧张素Ⅱ受体拮抗剂替米沙坦2mg／kg组（T1组）、替米沙坦5mg／kg组（T2组）、替米沙坦10mg／kg组（T3组）。采用坐骨神经慢性压迫性损伤法建立神经病理性痛模型。s组只暴露坐骨神经，但不结扎。T1组、T2组和T3组于术后第1天，分别经胃灌注替米沙坦2、5和10mg／kg，1次／d，连续14d，S组和NP组经胃灌注等容量生理盐水。分别于术前ld和术后3、7、14d时测定机械痛阈和热痛阈。结果与S组相比，NP组、T1组、T2组和T3组术后机械痛阈和热痛阈降低（P〈0．05）；与NP组相比，Tl组、T2组和T3组术后机械痛阈和热痛阈升高（P〈0．05）；与T1组相比，T2组和T3组术后机械痛阈和热痛阈升高（P〈0．05）；T1组与T3组机械痛阈和热痛阈相比差异无统计学意义（P〉0．05）。结论血管紧张素Ⅱ受体参与了大鼠神经病理性痛的形成。

Objective To evaluate the role of angiotensinⅡ receptors in the development of neuropathic pain （NP） in rats. Methods Seventy-five male Sprague-Dawley rats, weighing 230-270 g, were randomly divided into 5 groups （n = 15 each） using a random number table： sham operation group （group S）, group NP, telmisartan （angiotensin 11 receptor antagonist） 2 mg group （group T1）, telmisartan 5 mg group （group T2 ）, and telmisartan 10 mg group （group T3 ）. NP was induced by chronic constrictive injury （CCI） in chloral hydrate- anesthetized rats. The sciatic nerve was exposed and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 silk thread. In S group, the sciatic nerves Were exposed but not ligated. Telmisartan 2, 5 and 10 mg/kg were perfused via stomach once a day for 14 consecutive days in T1 , T2 and T3 groups, respectively, while the equal volume of normal saline was given instead of telmisartan in S and NP groups. Mechanical and thermal pain thresholds were measured at 1 day before CCI and 3, 7 and 14 days after CCI in each group. Results The mechanical and thermal pain thresholds were significantly decreased after CCI in NP, Tl , T2 and T3 groups as compared with group S. The mechanical and thermal pain thresholds were significantly increased after CCI in T1 , T2 and T3 groups as compared with group NP. The mechanical and thermal pain thresholds were significantly higher after CCI in T2 and T3 groups than in group T1 There was no significant difference in the mechanical and thermal pain thresholds between T2 and T3 groups. Conclusion Angiotensin Ⅱ receptors are involved in the development of NP in rats.