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出 处:《中华麻醉学杂志》2014年第7期833-835,共3页Chinese Journal of Anesthesiology
摘 要:目的 评价氧化应激在罗哌卡因诱发大鼠脊髓神经毒性中的作用.方法 清洁级雄性SD大鼠,体重250 ~ 320 g,3月龄,取L5,6间隙行鞘内置管,选择鞘内置管成功的大鼠90只,采用随机数字表法,将其分为3组(n=30):对照组(C组)、罗哌卡因组(R组)和抗氧化剂Tempol组(T组).R组和T组鞘内注射1%罗哌卡因1.2 μg/g,每次间隔1.5h,共8次,C组以等容量的生理盐水替代.T组分别于末次罗哌卡因注药结束后4、8、12、24、48、72 h时鞘内注射Tempol 20 μg/g.于罗哌卡因注药结束后1、3、5、7、14 d(T1-5)时处死,取脊髓腰膨大组织,行TUNEL染色,观察细胞凋亡情况;采用分光光度计比色法测定SOD活性,改良硫代巴比妥酸光电比色法测定MDA含量.结果 与C组比较,R组和T组细胞凋亡指数、脊髓MDA含量升高,SOD活性降低(P<0.05);与R组比较,T组细胞凋亡指数、脊髓MDA含量降低,SOD活性升高(P<0.05).结论 氧化应激参与了罗哌卡因诱发大鼠脊髓神经毒性损伤的发展.Objective To evaluate the role of oxidative stress in the spinal neurotoxicity induced by ropivacaine in rats.Methods Ninety pathogen-free male Sprague-Dawley rats,weighing 250-320 g,aged 3 months,in which intrathecal catheter was successfully implanted into L5,6 interspace without complications,were randomly divided into 3 groups (n =30 each) using a random number table:control group (group C),ropivacaine group (group R),and antioxidant Tempol group (group T).The rats received 1% ropivacaine 1.2 μg/g for 8 times at 1.5 h intervals through the catheter in R and T groups,while the rats received the equal volume of normal saline instead in group C.In T group,Tempol 20 μg/g was injected intrathecally at 4,8,12,24,48 and 72 h after the last injection of ropivacaine.The rats were sacrificed at 1,3,5,7 and 14 days after the end of ropivacaine injection,and their lumbar enlargements were removed for TUNEL staining to detect the cell apoptosis.SOD activity was determined by colorimetry and MDA content was measured using TBA photoelectric colorimetry.Apoptosis index was calculated.Results Compared with group C,apoptosis index and MDA content were significantly increased,and SOD activity was decreased in R and T groups.Compared with group R,apoptosis index and MDA content were significantly decreased,and SOD activity was increased in group T.Conclusion Oxidative stress is involved in the development of spinal neurotoxicity induced by ropivacaine in rats.
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