Intestinal pathophysiological mechanism of bacterial translocation and endotoxemia in rabbits with acute spinal cord injury
- VernacularTitle:急性脊髓损伤后家兔肠道菌群移位和内毒血症的肠道病理生理机制
- Author:
Chunhong BAI
;
Shali WANG
;
Hong AN
;
Dianming JIANG
;
Hai NIE
;
Leilei LI
- Publication Type:Journal Article
- Keywords:
spinal cord injury;
intestinal tract dysfunction;
bacterial translocation;
endotoxemia;
pathophysiological mechanism
- From:Journal of Third Military Medical University
1988;0(06):-
- CountryChina
- Language:Chinese
-
Abstract:
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 middle 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 interepithelial 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 (P0.05). 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 translocation and endotoxemia.
