摘要
目的 :研究老年肺炎的小肠损伤病理生理特点。方法 :复制肺炎双球菌肺炎大鼠模型 ,分为青年和老龄对照组及模型组。主要观察肺脏和小肠组织含水量 ,小肠组织 6酮前列腺素 F1α(6 keto PGF1α)、血栓素B2 (TXB2 )、一氧化氮 (NO)、丙二醛 (MDA)含量及超氧化物歧化酶 (SOD)活性。结果 :肺炎大鼠的肺组织损伤明显 ,肺脏和小肠组织含水量增高。青年模型组和老龄模型组小肠组织 6 keto PGF1α含量、SOD活性的降低和 TXB2 、NO、MDA含量的增高均较青年对照组和老龄对照组显著。与青年对照组比较 ,老龄对照组 SOD活性降低 ,MDA含量升高。老龄模型组 SOD活性的降低和 MDA含量的增高较青年模型组显著。结论 :前列腺素及自由基介导的损伤参与肺炎小肠组织损伤的发生和发展。由于增龄变化 ,肺炎老龄大鼠小肠自由基损伤较青年大鼠尤为严重。
Objective: To study the pathogenic mechanism underlying intestinal injury in the aged rat with pneumonia. Methods: The model of rats with Pneumococcus pneumonia was reproduced, and animals were divided into young control group (YCG), young model group (YMG), aged control group (ACG) and aged model group (AMG). The pathological change of lung tissue and intestine, contents of intestinal 6-keto-prostaglandin F 1α(6-keto-PGF 1α), thromboxane B 2(TXB 2), nitric oxide(NO), malondialdehyde(MDA) and superoxide dismutase (SOD) activity were determined in various groups. Results: The lung and intestinal injury in AMG was more serious than that in the YMG. The decreases in SOD activity and 6-ketoPGF 1α content, the increases in contents of TXB 2, NO, MDA in the YMG and the AMG were obvious than those in the YCG and the ACG respectively. The decrease in SOD activity and increase in MDA content were obvious in the ACG than those in the YCG. In addition, the decrease in SOD activity and increase in MDA content in the AMG were significant compared with those in the YMG. Conclusion: The prostaglandin metabolism and the free radical injury might be in the pathogenesis of intestinal injury in the aged rats with pneumonia. The intestinal injury induced by free radical in aged rats with pneumonia appears to be more obvious with ageing.
出处
《中国危重病急救医学》
CAS
CSCD
2003年第10期618-621,共4页
Chinese Critical Care Medicine
基金
河南省高校创新人才基金资助项目 ( 2 0 0 0 10 )
关键词
肺炎
大鼠
肺脏
小肠
前列腺素
一氧化氮
自由基
老年
pneumonia
rats
lung
intestine
prostaglandin
nitric oxide
free radical
aged
