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作 者:李永荣[1] 郭贵林[1] 尹逊华[1] 安虹[1] 姚德厚[1]
机构地区:[1]成都军区总医院
出 处:《中国病理生理杂志》1999年第2期167-169,共3页Chinese Journal of Pathophysiology
摘 要:目的:观察利多卡因对兔注射内毒素24h后的治疗效应。方法:用日本大耳白兔随机分为对照组、大肠杆菌内毒素(ET)组和ET注入后24h+利多卡因(lidocaine)组。用酶联免疫法和硫代巴比妥酸反应法测量血浆和支气管肺泡灌洗液(BALF)中TNFα和MDA含量。结果:免静注ET后24h再静注利多卡因,于静注利多卡因后3、5h,血浆和BALF中TNFα和MDA含量显著降低,血中性粒细胞数目明显回升。肺湿干重比值和BALF中性粒细胞数、白蛋白含量、C3a、C5a浓度无明显变化。结论:内毒素肺损伤后(注ET后24h)用lidocaine仍可抑制脂质过氧化反应和炎症介质的释放。AIM:To investigate the therapeutic effects of lidocaine on the later phase of endotoxin-induced lung injury in rabbits. METHODS:Japan white rabbits were randomly assigned to receive one of the three treatments: infusion of saline (control group), infusion of Escherichia coli endotoxin (ET group), the later phase of endotoxin-induced lung injury with lidocaine treatment (ET+lidocaine group). The tumor necrosis factor-α(TNFα) and malondialdehyde (MDA) contents in plasma and bronchoalveolar lavage fluid (BALF) were analysed by ELISA and Satrh TBA method respectively.RESULTS:The later phase of endotoxin-induced lung injury with lidocaine atteuated the changes of TNFα and MDA contents in plasma and BALF. The wet-to-dry weight ratio in the lung did not change and neutropils cell counts, albumin, C3a and C5a concentration in BALF did not change significantly as compared with ET group. CONCLUSION:In the later phase of endotoxin-induced lung injury lidocaine still inhibited lipoperoxidation and releases of the inflammatory mediators, and attenuated endotoxin-induced lung injury in rabbits.
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