[Delayed fluid resuscitation induced bacterial translocation after lethal thermal injury: role of oxygen free radical injury of intestinal mucosa].

The Present investigation was undertaken to examine the effect of delayed fluid resuscitation (DFR), after lethal thermal injury on oxygen free radical (OFR) injury of intestinal mucosa and its relationship to bacterial translocation. Four groups of gnotobiotic rats with 5 strains of bacteria were studied: sham injury group (control) (n = 6): early fluid resuscitation (EFR) group (n = 24) receiving resuscitation (Parkland) immediately after scald (40% TBSA, third degree); DFR group (n = 24) receiving resuscitation 6 hours after scald; treatment group (n = 12), rats with DFR receiving VitE and VitC treatment before resuscitation 12, 24, 48 and 72 hours after injury, animals (n = 6, at each point) were sacrificed. Plasma endotoxin level, mucosal SOD, GSHPx, MDA and diamine oxidase (DAO) of ileum were determined, and cultures of the mesenteric lymph nodes (MLN), liver, spleen, heart, lung, kidney and blood were done. The level of mucosal MDA and plasma endotoxin and the incidence of bacteria translocation (IBT) to tissues were significantly higher and mucosal SOD, GSHPx, DAO activity significantly lower in DFR group as compared with that in EFR group at most of the time points. In DFR group, mucosal MDA content was negatively correlated with mucosal DAO activity, which correlated positively with plasma endotoxin level and IBT. After treatment with VitE and VitC, mucosal MDA content was decreased, plasma endotoxin level and IBT were significantly decreased, and mucosal DAO activity was significantly increased. Our data indicated that DFR in cases of burn shock can result in OFR injury of intestinal mucosa, disrupting mucosal barrier and promoting translocation of intestinal bacteria and endotoxin.