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作 者:段清川[1] 刘俊秀[1] 方祎[1] 马芙蓉[1] 程翰俊[2] 毛兰群[2]
机构地区:[1]北京大学第三医院耳鼻咽喉科,北京100191 [2]中国科学院化学研究所,北京100190
出 处:《中国耳鼻咽喉头颈外科》2013年第2期102-104,共3页Chinese Archives of Otolaryngology-Head and Neck Surgery
基 金:国家自然科学基金项目(21272018);国家自然科学基金重大研究计划(90813032);北京市自然科学基金(7112144)联合资助
摘 要:目的探讨水杨酸钠诱导动物产生耳鸣时神经递质在中枢发病机制中的作用。方法将28只Wistar大鼠(280~320 g)随机分为3组:水杨酸钠组(n=12)使用水杨酸钠腹腔注射(350 mg/kg)制造耳鸣模型;水杨酸钠+利多卡因组(n=12)于水杨酸钠诱导耳鸣后给予利多卡因脑区局部微灌注治疗;对照组(n=4)使用等量生理盐水腹腔注射。利用微透析技术,在耳鸣动物活体清醒状态下,研究水杨酸钠对听觉中枢皮层的抗坏血酸变化及利多卡因对抗坏血酸影响。结果腹腔注射10%水杨酸钠(350 mg/kg)引起听皮层抗坏血酸水平显著性升高,最高达到基础值的(516±162)%;通过局部脑组织灌流,利多卡因能显著降低抗坏血酸的升高趋势(F=64.649,P<0.001);对照组并未引起任何显著改变。结论腹腔注射水杨酸钠后,听觉中枢皮层抗坏血酸水平显著升高,可能与水杨酸诱导的耳鸣产生有关,给予利多卡因干预后听皮层抗坏血酸升高趋势降低可能与其抑制耳鸣的作用机制有关。OBJECTIVE To study neurotransmitter changes in the auditory cortex (AC) of rat tinnitus model induced by salicylate for understanding the action of salicylate on the auditory system and the neurological mechanisms of salicylate-induced tinnitus. METHODS Twenty eight Wistar rats weighing 280N300 grams were randomly divided into saline treatment group (n=4) , salicylate treatment group (n=12) , and salicylate+lidocaine treatment group (n=12) , Using in vivo microdialysis technique coupled with on-line electrochemical detection, the ascorbic acid release in AC was monitored and the effects of lidocaine on ascorbic acid changes in AC were examined in salicylate-induced tinnitus animal models. RESULTS Salicylate (350 mg/kg i.p., n=12) produced an significant increase of ascorbic acid in the AC (up to 516%± 162% of baseline) . The increase of ascorbic acid level in salicylate + lidocaine group were significantly depressed in AC after local infusion (F=64.649, P〈 0.001) . In contrast, saline did not produce any significant changes. CONCLUSION The significant increase of AC ascorbic acid concentration after application of salicylate may be involved in tinnitus generation. The suppression of lidocaine to tinnitus may be associated with the depression of ascorbic acid level in AC in tinnitus generation.
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