摘要
目的 观察失血性休克后肠道损伤情况与过氧化反应和TNF、IL 6的变化。方法 利用大鼠失血性休克模型 (30mmHg、70min) ,在复苏后 0、2、6、12、2 4、和 48h检测血液和小肠组织的过氧化物歧化酶 (SOD)活性 ,丙二醛 (MDA)、TNF和IL 6含量 ,以及小肠的病理改变和肠道菌移位情况。结果 大鼠血清MDA值在复苏后 0~ 2h升高 ,SOD活性多数时间点均升高 ;小肠MDA值在 0~ 2 4h升高 ,SOD活性 0~ 12h降低。血清TNF含量在 6~ 48h升高 ;小肠在 0~ 12h升高。IL~ 6含量无明显变化。小肠粘膜在复苏后 2h有明显的上皮脱落 ,6~ 12h ,可见细菌侵入粘膜层 ,6~ 48h ,在肠系膜淋巴结等脏器中检出肠道菌。结论 大鼠失血性休克后肠粘膜SOD合成能力的降低或活性抑制可能是加重局部损伤的机制之一。
Objective To observe the injury and permeability of intestine, together with the changes of peroxidation and TNF and IL 6 concentrations after hemorrhagic shock in rats. Methods At 0, 2, 6, 12, 24 and 48 hours after being subjected to sham shock, or 70 minutes of 30mmHg shock, rats were sacrificed. The SOD activity and the MDA, TNF and IL 6 concentrations in serum and intestine were detected, the histology and bacteria translocation of intestine were also observed. Results The serum MDA concentration was increased at 0-2h after shock and SOD activity was increased almost all the detected time. In the intestine, the MDA concentration increased at 0-24h, and SOD activity decreased at 0-12h. The serum TNF concentration was increased at 6-48h after shock while increased at 0-12h in intestine. No change was observed of IL 6 concentration in both serum and intestine. Extensive sheding of mucosa epithelia were observed at 2h after shock and the bacteria were observed at 6-12h in lamina propria. The indigenous bacteria of intestine were detected at mesenteric lymph nodes and other visceral organs at 6-48h after shock. Conclusion The SOD activity decrease was one of the reasons in intestine injury after hemorrhagic shock. The early phase increase of serum TNF came from the injured intestine.
出处
《中国实验动物学报》
CAS
CSCD
2001年第3期164-167,共4页
Acta Laboratorium Animalis Scientia Sinica
基金
"九五"全军医药卫科研基金 (96Q10 2 )