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.


METHODS
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.


METHODS
University animal laboratory.


METHODS
Male Wistar rats, weighing between 300 and 350 g.


METHODS
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.


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.
Kahlke
Volker
V
Department of General Surgery, University of Kiel, Kiel, Germany.
Fändrich
Fred
F
Brötzmann
Kerstin
K
Zabel
Peter
P
Schröder
Jörg
J
D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D018988:Bacterial Translocation; D003666:Decontamination; D004064:Digestive System / Q000187:drug effects*; D005243:Feces / Q000382:microbiology; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D009092:Mucous Membrane / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012771:Shock, Hemorrhagic / Q000097:blood* / Q000188:drug therapy; D013154:Spleen / Q000187:drug effects / Q000378:metabolism; D014031:Tobramycin / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D000900:Anti-Bacterial Agents; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D014031:Tobramycin