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Volume 17 Supplement 4

Sepsis 2013

  • Poster presentation
  • Open Access

Interruption of the intestinal immune route to the systemic circulation associated with early hyperhydration minimized splanchnic microcirculation damage and improved sepsis survival

  • 1,
  • 2,
  • 1 and
  • 1
Critical Care201317 (Suppl 4) :P72

  • Published:


  • Sepsis Group
  • Lymph Duct
  • Potential Therapeutic Application
  • Microcirculation Dysfunction
  • Sidestream Darkfield


Considering that the communication of the intestinal immunity with the systemic bloodstream can be a relevant adjuvant factor in the amplification of the host systemic inflammatory response and subsequent multiple organ dysfunction in sepsis, we aimed to evaluate the effect of the obstruction of the mesenteric lymph duct (OMLD) associated with massive fluid therapy in the early phase of sepsis and severe sepsis models.

Materials and methods

Adult Wistar-EPM rats were submitted to 108 (S8) or 109 (S9) CFU/ml Escherichia coli inoculum intravenously (i.v.) (DL80 within 26 hours), and were treated with hyperhydration (HH) with or without previous OMLD (n = 5/group). Control group were naïve animals (N) and animals submitted to HH or sepsis only. The mortality of groups was followed up to 30 days after experiments and microcirculation monitoring was observed at 6 hours post sepsis induction by videomicroscopy (sidestream darkfield imaging (SDF)).


The effect of OMLD + HH reduced significantly the sepsis mortality rate: S8 (60% to 14.5%) and S9 (80% to 60%). Besides, the liver and kidney microcirculatory features were better preserved as compared with untreated sepsis groups under video-microscopy (SDF) monitoring. (Figure 1).
Figure 1
Figure 1

Splanchnic organ's microcirculation following 6 hours after sepsis or HH procedures by SDF monitoring: (a) HH; (b) S8 + OMLD + HH; (c) S9 + OMLD + HH.


These preliminary findings showed that both HH and OMLD have a potential therapeutic application in sepsis by minimizing the splanchnic organ's microcirculation dysfunction.



Grant number 2011/204014, São Paulo Research Foundation (FAPESP).

Authors’ Affiliations

Department of Surgery, Federal University of São Paulo, Brazil
Department of Pediatrics, Federal University of São Paulo, Brazil


© Dulcini et al.; licensee BioMed Central Ltd. 2013

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