摘要
目的探讨家兔脊髓损伤后肠道菌群移位和内毒血症的肠道病理生理机制。方法建立兔脊髓损伤性截瘫模型,12只家兔行脊髓损伤前后胃肠道电生理和压力测定。另外24只家兔分为:正常对照组(6只)和实验组(18只),在无菌条件下,采集门静脉血进行内毒素定量测定和细菌培养,肠系膜淋巴结作细菌培养并鉴定。取实验组和对照组各动物的小肠、结肠行HE染色检查观察肠黏膜病理变化,小肠行电镜检查观察肠黏膜上皮细胞病理变化。结果脊髓损伤后,发现胃肠道生物电改变明显,以结肠为重。中远段结肠的蠕动明显减少,部分时段甚至消失。早期小肠和结肠黏膜下充血和黏膜上皮细胞水肿,随后,黏膜上皮间隙增宽,细胞崩解,导致肠黏膜屏障破坏。血清内毒素含量从24h就开始增高,到72h差异显著(P<0.05)。门静脉血与肠系膜淋巴结各阶段细菌培养阳性率均较高,无统计学差异(P>0.05)。结论急性脊髓损伤后,中远段结肠的蠕动功能障碍导致排便障碍、细菌过度增长与入侵、影响血运等一系列破坏因素而加速肠黏膜屏障破坏为肠道菌群移位和内毒血症的主要病理生理机制。
Objective To investigate the intestinal pathophysiological mechanism of bacterial translocation and endotoxemia in rabbits with acute spinal cord injury （SCI）. Methods Paraplegia was induced by injuring the spinal cord of 30 rabbits by the method of Fehlings. Twelve rabbits were used for recording the changes of gastrointestinal （GI） electrophysiology and colon pressure. The left 18 rabbits were experimental group and were killed in 24, 48 and 72 h after injury. The other 6 rabbits served as normal group. Under aseptic condition, samples of blood and mesenteric lymph node were collected for bacterial cultures and endotoxin detection. The small intestines were observed by light and electron microscopy. The colons were inspected by light microscopy. Results After SCI, the electrophysiology of the GI tract was changed especially at the middie and distal colon. The peristalsis of the middle and distal colon was reduced and sometimes even disappeared. In the early stage, the main pathology was hyperemia of blood vessel and infiltration of inflammatory cells. The interepithetial tight junctions became wider and the columnar epithelium was disintegrated. All of the pathological changes may lead to the destruction of the intestinal barrier. The endotoxin level were increased since 24 h after SCI and had statistically significant difference compared with that at 72 h （ P 〈 0.05 ）. The positive rates in blood and mesenteric lymph nodes at 24, 48 and 72 h were very high, but there was no significant difference among them （P 〉 0.05）. Conclusion After SCI, the middle and distal colon dysfunction induces constipation, bacterial overgrowth, and blood flow congestion. These factors may accelerate the destruction of the intestinal barrier and lead to bacterial transloeation and endotoxemia.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2010年第6期580-583,共4页
Journal of Third Military Medical University
关键词
脊髓损伤
肠道功能障碍
细菌移位
内毒素血症
病理生理机制
spinal cord injury
intestinal tract dysfunction
bacterial translocation
endotoxemia
pathophysiological mechanism
