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作 者:李泽信[1] 李荣[2] 薛会朝[1] 刘江伟[3] 张永久[3] 冯德元[3]
机构地区:[1]新乡医学院第一附属医院普外科,河南卫辉453100 [2]新乡医学院,河南新乡453003 [3]兰州军区乌鲁木齐总医院普外科,新疆乌鲁木齐830000
出 处:《现代生物医学进展》2009年第17期3266-3268,共3页Progress in Modern Biomedicine
基 金:兰州军区医药卫生科研基金资助项目(LXH-2005019)
摘 要:目的:探讨血浆内毒素在腹部火器伤肠管穿透后肝损伤中的作用。方法:健康长白仔猪42头随机等分为对照组和伤后1h、2h、4h、8h、12h和24h组,实验组建立腹部火器伤肠管穿透模型后,用显色基质鲎试剂法检测各组血浆内毒素水平,用免疫组化图像分析法测定各组肝内TNF-α含量,同时测定血清中ALT水平变化情况,在光镜下观察各组肝脏组织学变化。结果:伤后各组血浆内毒素水平、肝组织TNF-α的表达及血清ALT水平均明显高于对照组(P<0.05)。血浆内毒素水平于伤后8h出现高峰,伤后12h仍维持在高峰值水平;伤后各组出现逐渐加重的肝细胞水肿、变性、坏死,肝组织TNF-α含量及血清ALT水平均于伤后2h和12h出现2个高峰。相关分析表明,伤后肝组织TNF-α含量与血浆内毒素及血清ALT水平均呈正相关(r值分别为0.802、0.895,P<0.05)。结论:腹部火器伤肠穿孔后内毒素血症可引起肝内TNF-α含量增高来介导继发性肝损伤的发生。Objective: To investigate the role of plasma endotoxin in the mechanism of liver injury after intestinal perforations duing to abdominal firearm wound. Methods: 42 Chang-Bai piglets were randomized into 7 groups:control group and wounded lhour group, 2hour group, 4hour group, 8hour group, 12hour group, 24hour group. The model of intestinal perforations duing to abdominal firearm wound was established in wounded groups. Levels of plasma endotoxin was measured by ehromogenic limulus amehoeyte lysate test.Hepatic TNF-α content was measured by immunohistochemieal staining and image analysis in all groups. And serum ALT were determined at the same time. The alterations of hepatic tissue were observed under light microscope. Results: Levels of plasma endotoxin, hepatic TNF-α content, serum ALT in wounded groups were all significantly elevated compared to control group (P〈0.05). Plasma endotoxin reached the peak in 8h group,and it was still at the peak level in 12h group. Hepatocyte edema, metamorphosis, necrosis were gradually aggravated from lh group to 24h group. Content of both hepatic TNF-α and serum ALT appeared two peaks in 2h group and 12h group. In addition, the level of hepatic TNF-α was positively correlated with plasma endotoxin and serum ALT (r=0.802 and 0.895 P〈0.05). Conclusion: After intestinal firearm wound, the activity of endotoxemia provokes hepatic TNF-α increase and TNF-α may mediate subsequent liver injury.
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