右美托咪定对大鼠脊髓缺血再灌注损伤的影响及其机制.docVIP

DOI：10.16016/j.1000-5404.201409078 右美托咪定对大鼠脊髓缺血-再灌注损伤的影响及其机制 王中权，王 府，冉龙宽，田泽丹，陈玉培（400010 重庆，重庆医科大学附属第二医院麻醉科） [摘要] 目的 观察右美托咪定对大鼠脊髓缺血-再灌注损伤的影响，并探讨其可能的机制。方法 96只成年SD大鼠按随机数字表法分为4组（n=24）：假手术组（S组）、缺血再灌注组（IR组）、缺血再灌注右美托咪定组（DEX组）和缺血再灌注右美托咪定育亨宾组(DY组)，每组再分为灌注后12、24、4872 h 4个亚组（n=6）。采用临床常用的首次负荷量加持续微量泵给药方式予以右美托咪定和育亨宾处理，并通过改良Zivin法阻断双肾间腹主动脉建立脊髓缺血-再灌注损伤模型，采用BBB法对大鼠运动功能评分，HE染色观察大鼠脊髓病理学改变（L4-6），免疫组化观察脊髓Bax、Bcl-2TUNEL法计数脊髓细胞凋亡率，Western bolt检测Caspase3表达。结果 与IR组比较，DEX组和DY组BBB运动评分升高，HE染色病理损伤明显减轻，TUNEL染色细胞凋亡率下降，免疫组化Bcl-2升高，Bax降低(P0.05)，Western blot显示caspase3表达减少；与DEX组比较，DY组BBB运动评分降低，HE染色病理损伤加重，TUNEL染色细胞凋亡率升高，免疫组化Bcl-2降低，Bax升高（P0.05），Western blot显示caspase3表达增加。结论 右美托咪定对大鼠脊髓缺血-再灌注损伤具有明显的保护效应，其机制与激动α2肾上腺素受体，增加FAK磷酸化，并上调Bcl-2表达，下调Bax和caspase3表达的抗细胞凋亡作用有关。 [关键词] 缺血再灌注损伤；右美托咪定；育亨宾；脊髓 [中图法分类号] R965；R744.1；R364 [文献标志码] A Effect of dexmedetomidine on spinal cord ischemia-reperfusion injury in rats Wang Zhongquan, Wang Fu, Ran Longkuan, Tian Zedan, Chen Yupei (Department of Anesthesiology, Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400010, China) [Abstract] Objective To investigate the effect of dexmedetomidine on spinal cord ischemia-reperfusion injury in rats, and explore possible mechanism. Methods A random number table method was used to divide 96 adult SD rats into four groups (n = 24): a sham operation group (S), an ischemia-reperfusion group (IR), a dexmedetomidine treatment group (DEX), and a dexmedetomidine and yohimbine combination treatment group (DY), and each group was further divided into four subgroups (n = 6) according to time points (12 h, 24 h, 48 h and 72 h) after ischemia-reperfusion injury. After the spinal cord ischemia-reperfusion injury model was established with an improved Zivin method, the motion function of the hind limbs was evaluated by BBB scale, and L4-6 spinal cord pathological changes were observed by HE staining. The expressions of Bcl-2 and Bax were examined by immunohistochemical staining, and the expression of caspase 3