摘要
目的 研究老年肺炎的小肠损伤病理生理特点。方法 复制大肠杆菌肺炎模型 ,分为青年对照组和模型组、老龄对照组和模型组。主要观察肺脏和小肠组织病理改变和含水量 ,小肠组织 6 -Keto -PGF1α、TXB2 、NO和MDA含量及SOD活性。结果 肺炎鼠的肺、小肠组织损伤明显和含水量增高 ,老龄大鼠组织损伤较青年大鼠严重。与青年对照组比较 ,青年模型组SOD活性和 6 -Keto -PGF1α含量降低 ,TXB2 、NO、MDA含量较高。老龄对照组NO含量降低和MDA含量增高较青年对照组显著。老龄模型组SOD活性、6 -Keto-PGF1α含量的降低和NO、MDA、TXB2 含量的增高较老龄对照组显著。与老龄模型组比较 ,青年模型组MDA、NO含量降低和SOD活性升高。结论 前列腺素及自由基介导的损伤参与肺炎的小肠组织损伤发生发展。由于增龄变化 。
Objective To study the pathogenic mechanism on intestinal injury in the aged rat with pneumonia.Methods Duplicated the model of rats with escherihia coli pneumonia and divided rats into young control group (YCG),young model group (YMG),aged control group (ACG) and aged model group (AMG).It was observed that the pathological change of lung tissue and intestine,the content of intestinal 6-Keto-PGF 1α ,TXB 2,NO,MDA and SOD activity.Results The lung and intestinal injury in AMG was more serious than that in the YMG.The decrease of SOD activity and 6-Keto-PGF 1α content,the increase of content of TXB 2,NO,MDA in the YMG than those in the YCG.The decrease of NO level and increase of MDA content was obvious in the ACG than those in the YCG.The decrease of SOD activity and 6-Keto-PGF 1α content,the increase of content of TXB 2,NO,MDA in the AMG than those in the ACG.Compared with those in the AMG,the activity of SOD increased and the content of MDA and NO decreased in the YMG.Conclusions The PG metabolism and the FR injury concerned with the pathological development in intestinal injury in the aged rat with pneumonia.The intestinal injury induced by FR in aged rats with pneumonia was more obvious with ageing. [
出处
《中国急救医学》
CAS
CSCD
北大核心
2001年第8期438-441,共4页
Chinese Journal of Critical Care Medicine
基金
河南高校创新人才基金 (2 0 0 0 -10 )
关键词
肺炎
老年大鼠
肺脏
小鼠
前列腺素
一氧化氮
自由基
Pneumonia
Rats
Lung
Intestine
Prostaglanda
Nitric oxide
Free radical
Aged
