Selective decontamination of the digestive tract: impact on cytokine release and mucosal damage after hemorrhagic shock.

OBJECTIVE

To determine if selective decontamination of the digestive tract (SDD) influences the proinflammatory immune response of the gut after hemorrhage.

DESIGN

Random assignment to either unmanipulated control after 7 days of SDD or conventional rat chow, or hemorrhagic shock group after the same time of conventional rat chow or SDD.

SETTING

University animal laboratory.

SUBJECTS

Male Wistar rats, weighing between 300 and 350 g.

INTERVENTION

Animals of the control group were not manipulated until organ harvesting, whereas animals of the hemorrhagic shock group were bled to 30 +/- 5 mm Hg for 90 mins by withdrawal/reinfusion of shed blood and were resuscitated by Ringer's lactate equivalent to the shed blood volume.

MEASUREMENTS AND MAIN RESULTS

Rats were killed after resuscitation (hemorrhagic shock group) or completed feeding (control group). Whole portal and caval blood was obtained, and splenic macrophages and gut mononuclear cells were harvested to measure supernatant tumor necrosis factor-alpha and IL-6 by bioassay. Mesenteric lymph nodes were obtained to determine bacterial translocation, and a histologic specimen was taken from the distal ileum. Feces were harvested to examine the effect of SDD. SDD eliminated Gram-negative enteric bacteria and had no influence on mucosal damage or on bacterial translocation in control animals and animals after hemorrhage. In animals receiving conventional rat chow, hemorrhagic shock led to significantly (p <.05) elevated lipopolysaccharide-stimulated proinflammatory cytokine (tumor necrosis factor-alpha and interleukin-6) release in whole portal blood, splenic macrophages, and gut mononuclear cells compared with the control group without shock. In contrast, hemorrhagic shock after SDD led to suppressed or unchanged cytokine release compared with unmanipulated animals receiving SDD. However, SDD itself induced significant (p <.05) cytokine release in these organs. Furthermore, plasma concentrations of tumor necrosis factor-alpha and interleukin-6 were significantly (p <.05) elevated in animals after hemorrhage and SDD compared with animals after hemorrhage alone.

CONCLUSIONS

Hemorrhagic shock led to significant cytokine release. In contrast, cytokine release after hemorrhage and SDD was unchanged or suppressed. Furthermore, in control animals without hemorrhagic shock, SDD induced significant cytokine release. Therefore, selective decontamination of the gut, as practiced in some patients, may induce additional proinflammatory cytokine release, which can add to the proinflammatory burst in case of a complication such as hemorrhagic shock.