期刊文献+

攻下药物对重型急性胰腺炎急性肺损伤模型大鼠的治疗作用观察 被引量:2

Study of Gongxia Drug's Treatment Effect on Acute Lung Injury Induced by Severe Acute Pancreatitis in Rats
下载PDF
导出
摘要 目的:观察急性重型胰腺炎急性肺损伤动物模型肺泡巨噬细胞计数、活性、分泌炎性细胞因子功能变化及药物对其影响。方法:制备大鼠重型胰腺炎模型,采取肺泡巨噬细胞做各项指标检测及病理学检查。结果:模型组病理表现为明显的肺损伤,大承气汤治疗效果最显著。模型组肺泡巨噬细胞计数、活性、分泌炎性细胞因子显著高于对照组(P<0-01) ,各治疗组显著低于模型组( P< 0-01) ,善得定抑制巨噬细胞分泌炎性细胞因子作用最强,大承气汤抑制巨噬细胞数量较显著。结论:肺泡巨噬细胞过度活化,过度分泌炎性细胞因子是重型急性胰腺炎急性肺损伤发病的重要原因之一。中药能控制过度的炎性反应状态。 To observe the macrophage's count,activity and functional change secreting inflammatory cytokin and the medicine's influence on the macrophages in the animal models with lung injury induced by severe acute pancreatitis.Methods:We improved the rat model employing the method of ACHO and made pathological examination of the rats executed of ACHO and made pathological examination of the rats exectuted after 72 hours,According to the method of Tian Zaishan,we collected alveoli macrophages and examined these indexes mentioned above.Results:The pathological manifestation of the model group showed obvious lung injury and the Dachengqi tang's protect effect is most significant.The indexes of model group are significantly higher than those of control group (P<0.01) and the indexes of treatment group are significantly lower than those of control group;The effect of Sandostatin's suppressing the macrophage's secreting inflammatory cytokin is most significant and the effect of Dachengqi tang's suppressing the macrophage's quantity is significant.Conclusion:The alveoli macrophage's excessive activation and secreting inflammatory cytokin excessively is one of the most important reasons of acute lung injury induced by acute severe pancreatitis.The Chinese traditional herbs have protecting effect on the damaged lung tissue by regulating excessive inflammatory reaction.
出处 《中国中西医结合外科杂志》 CAS 1999年第6期353-356,共4页 Chinese Journal of Surgery of Integrated Traditional and Western Medicine
关键词 重型 胰腺炎 肺损伤 大承气汤 中医药疗法 severe acute pancreatitis acute lung injury Dachengqi decoction
  • 相关文献

参考文献3

共引文献35

同被引文献40

引证文献2

二级引证文献9

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部