title: Influences of intestinal ligation on bacterial translocation and inflammatory response in rats with hemorrhagic shock: implications for damage control surgery.
abstract: Damage Control Surgery (DCS) treatment of rapid intestinal ligation to control the bowel spillage in severe abdominal trauma induces acute intestinal loop obstruction. The purpose of this study was to investigate the effects of intestinal ligation on bacterial translocation (BT) and inflammatory reaction under the condition of acute hemorrhagic shock and its probable pathophysiology. Escherichia coli TG1 labeled with green fluorescent protein was used to track BT by gavage to rats. Group Shock rats were subjected to hemorrhagic shock for 30 minutes. Group Shock+Ligation (Shock+L) rats were subjected to hemorrhagic shock and following intestinal ligation. We found that hemorrhagic shock alone or in combination with intestinal ligation caused not only morphological damage to ileal mucosa, but also induced BT and promoted release of TNF-alpha, IL-6, and IL-10 in serum and lymph. Ileal mucosa injuries and BT were significantly aggravated and cytokine levels in serum and lymph were significantly elevated in group Shock+L compared with group Shock. The positive proportions of bacterial culture and cytokine levels were significantly elevated in lymph compared with these in blood in both groups. By fluorescence microscope and XbaI restriction digestion analysis, we elucidated that the bacteria isolated from extraintestinal organs were the same bacteria we gavaged to the rats. We first confirmed that DCS treatment of rapid intestinal ligation under the condition of acute hemorrhagic shock leads to aggravated intestinal mucosa barrier injury and BT and elevated inflammatory response. The intestinal BT and immunoinflammatory factors may act through or mainly through lymph route.
authors.affiliation: Department of Surgery, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province, China.
authors.forename: Pengfei
authors.initials: P
authors.lastname: Wang
authors.forename: Xiaowei
authors.initials: X
authors.lastname: Wei
authors.forename: Yousheng
authors.initials: Y
authors.lastname: Li
authors.forename: Jieshou
authors.initials: J
authors.lastname: Li
mesh_terms: D000668:Ampicillin Resistance / Q000235:genetics; D000818:Animals; D016207:Cytokines / Q000097:blood / Q000378:metabolism; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics / Q000472:pathogenicity; D049452:Green Fluorescent Proteins / Q000235:genetics; D007249:Inflammation / Q000209:etiology* / Q000503:physiopathology; D007422:Intestines / Q000293:injuries / Q000382:microbiology* / Q000601:surgery*; D008026:Ligation; D008196:Lymph / Q000276:immunology / Q000382:microbiology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D011994:Recombinant Proteins / Q000235:genetics; D012771:Shock, Hemorrhagic / Q000150:complications* / Q000382:microbiology / Q000503:physiopathology / Q000601:surgery*
chemical_list: D016207:Cytokines; D011994:Recombinant Proteins; C485184:enhanced green fluorescent protein; D049452:Green Fluorescent Proteins