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作 者:胡森[1] 张立俭[1] 白慧颖[1] 包呈梅[1]
机构地区:[1]解放军总医院第一附属医院烧伤研究所休克与多器官障碍实验室,北京100048
出 处:《中国危重病急救医学》2009年第8期485-487,共3页Chinese Critical Care Medicine
基 金:全军“十一五”计划专项课题(062055)
摘 要:目的探讨电针足三里穴对脓毒症大鼠肠缺血和氧自由基损伤的保护作用。方法采用盲肠结扎穿孔术(CLP)制备大鼠脓毒症模型。雄性Wistar大鼠32只,随机分为CLP+电针足三里(CLP/EA)组、CLP+假电针(CLP/SEA)组、迷走神经切断+CLP+SEA(VA/CLP/SEA)组、VA+CLP+EA(VA/CLP/EA)组,每组8只。EA组持续针刺双侧足三里穴30min,刺激强度为2~3mA,2~100Hz;SEA组采用相同频率和强度刺激非经非穴(足三里外侧旁开0.5cm)30min;VA组于CLP前切断迷走神经。各组大鼠于CLP后6h测定空肠黏膜血流量(JMBF),处死动物取空肠组织,测定丙二醛(MDA)含量、黄嘌呤氧化酶(XOD)和二胺氧化酶(DAO)活性及肠组织含水量。结果与CLP/SEA组比较,CLP/EA组JMBF和DAO活性显著增加,XOD和MDA及肠组织含水量显著降低(P均〈0.05);VA/CLP/SEA组和VA/CLP/EA组JMBF和DAO活性显著降低,XOD和MDA水平显著升高,且组织含水量明显高于CLP/EA组(P均〈O.05)。VA/CLP/EA组与VA/CLP/SEA组各指标均无明显差异(P均〉0.05)。结论电针足三里可显著增加CLP大鼠JMBF和DAO活性,减轻肠组织水肿和脂质过氧化损伤;切断腹腔迷走神经能减轻或消除电针的作用,增强小肠组织过氧化反应,加重肠组织水肿和黏膜细胞损害。电针足三里穴对肠缺血和氧自由基损伤的保护机制可能与兴奋胆碱能通路有关。Objective To investigate the protective effect of electro-acupuncturing (EA) at Zusanli point (足三里穴) on sepsis induced ischemie and oxygen free radical intestinal injury in rats with sepsis. Methods Thirty-two male Wistar rats were used to reproduce sepsis by cecal ligation and puncture (CLP), and they were randomly divided into four groups (each n = 8): CLP+EA (CLP/EA), CLP +sham EA (CLP/SEA), vagotomy+CLP+SEA (VA/CLP/SEA) and vagotomy+CLP+EA (VA/CLP/EA). Zusanli point was electro-acupunctured with constant voltage (2 - 100 Hz,2 mA for 30 minutes) immediately after CLP surgery. Abdominal vagotomy was performed in rats in VA/CL/SEA and VA/CLP/SEA groups. Six hours after CLP, the mueosal blood flow of jejunum (JMBF) was measured. Animals were sacrificed after 6 hours and specimens of jejunum were harvested for evaluation of malondialdehyde (MDA), xanthine oxidase (XOD), diamine oxidase (DAO) and assessment of the water content (WCR). Results JMBF and the activity of DAO of CLP/EA group were markedly higher, and the levels of XOD, MDA and WCR in jejunal tissue were obviously lower than those of CLP/SEA group (all P〈0. 05). The levels of JMBF and DAO of the VA/CLP/SEA group and VA/CLP/EA group were significantly lower, and XOD, MDA and WCR obviously higher than those of the CLP/EA group (all P〈0.05). There were no statistically differences in all above measurements between the VA/CLP/EA group and the VA/CLP/SEA group (aU P〉0. 05). Conclusion The results indicate that EA at Zusanli point obviously increased JMBF and DAO, and alleviated tissue edema and insult of intestinal mucosa. Vagotomy could weaken or eliminate the effects of EA. It is suggested that cholinergie anti-inflammatory pathway is one of the main mechanisms of intestinal protective effect of EA at Zusanli point.
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