Abstract
Objective
An experimental model of severe injury with great lethality was studied to define
the impact of bacterial translocation on survival and on inflammatory response.
Methods
Forty-one rabbits were divided into two groups: A, femur myotomy; and B, myotomy and
fracture of the femoral bone. Vital signs and survival were recorded. Serum circulating
endotoxins (lipopolysaccharides; LPS) were determined and tissue cultures were performed
at necropsy. A subgroup of animals was sacrificed at 48 h post injury; LPS was determined
in abdominal aorta and portal vein, apoptosis of spleen cells was assessed by flow
cytometry, and ex vivo production of tumor necrosis factor alpha by splenocytes was measured.
Results
Tissue bacterial burden was increased in animals that died early (i.e., within 48 h
after injury) versus rabbits that died later. Portal vein LPS at 48 h was increased in group B compared
with group A, whereas circulating LPS did not differ. No difference in apoptosis of
either lymphocytes or macrophages of the spleen was found in group B compared with
group A. Following stimulation with LPS or phytohemagglutinin, tumor necrosis factor
α production by splenocytes of group B was greater than that of group A.
Conclusions
Bacterial translocation primes enhanced proinflammatory responses and it is associated
with early death in severe trauma.
Keywords
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Article info
Publication history
Published online: August 05, 2013
Accepted:
July 11,
2013
Received in revised form:
July 11,
2013
Received:
March 25,
2013
Identification
Copyright
© 2013 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
