Title of article :
Role of gut-derived endotoxaemia and bacterial translocation in rats after thermal injury: effects of selective decontamination of the digestive tract
Author/Authors :
Y. -D. Yao، نويسنده , , Y. Yu، نويسنده , , Z. -Y. Sheng (C.Y. Sheng)، نويسنده , , H. -M. Tian، نويسنده , , Y. -F. Wang، نويسنده , , L. -R. Lu، نويسنده , , Y. Yu، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1995
Pages :
6
From page :
580
To page :
585
Abstract :
This study was performed to investigate: (1) the role of gut-derived endotoxin/bacterial translocation in the pathogenesis of sepsis, and (2) the possible effects of selective decontamination of the digestive tract (SDD) on mortality in rats following 40 per cent full-thickness scald injury. In the SDD-treated group, Enterobacteriaceae and yeasts were eradicated from the caecal mucosa, while the mucosal flora consisting of mainly anaerobes was well preserved, within 3 days. The incidence of bacterial translocation to the mesenteric lymph nodes (MLN) and viscerae was significantly lowered on postburn days 1, 3 and 5 (P< 0.05−0.01). Meanwhile, pretreatment with SDD resulted in reductions of the faecal endotoxin levels in different segments of intestinal tract to less than 0.5 per cent (0.04 – 0.45 per cent) of the untreated control; there was also a significant attenuation of the elevation of endotoxin concentrations in both portal and systemic blood. Intestinal diamine oxidase (DAO) activity returned to baseline on day 5 in rats receiving SDD but not in controls. The 5-day survival rate in the SDD-treated group was elevated by 26.7 per cent as compared with controls (P< 0.05). These data suggested that endotoxin/bacterial translocation took place early and commonly, which in turn contributed to postburn sepsis and mortality. SDD was effective in preventing gut origin endotoxaemia and bacterial translocation, and improving the survival rate in rats following severe thermal injuries.
Journal title :
Burns
Serial Year :
1995
Journal title :
Burns
Record number :
469428
Link To Document :
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