[Open abdomen management treatment of liver injury in rats with abdominal compartment syndrome and sepsis]

Zhonghua Wai Ke Za Zhi. 2011 Apr 1;49(4):335-40.
[Article in Chinese]

Abstract

Objective: To evaluate the open and closed management treatment of liver injury in rats with sepsis and abdominal compartment syndrome (ACS).

Methods: The sepsis and ACS rats (n = 72) were randomized divided into two groups. One group used closed management (n = 36), the other accepted the open abdomen management (n = 36). The rats were killed at 1, 6 h, 1, 3, 5, 7 d after operation. Blood was collected for liver function tests. Liver sections assessed pathologically and the expressions of Toll-like receptor 4 (TLR4), tumor necrosis factor (TNF)-α, interleukin (IL)-6, signal transducers actuators of transcription (STAT3) and suppressor of cytokine signaling 3 (SOCS3) of rat livers were examined by RT-PCR.

Results: The early stage after operation, TNF-α and IL-6 concentrations, STAT3 expressions in rat liver were higher in open abdomen rats than the closed management ones (P < 0.05). TLR4 and SOCS3 expressions were lower in open abdomen rats than the closed management ones (P < 0.05). Aspartate aminotransferase, alanine aminotransferase levels also was lower in open abdomen ones (P < 0.05).

Conclusions: The randomized study demonstrates that open abdomen management could improve liver regeneration in the early stage after operation. Also open abdomen could reduce inflammatory response by reducing TLR4 expressions.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Disease Models, Animal
  • Interleukin-6 / metabolism
  • Intra-Abdominal Hypertension / metabolism
  • Intra-Abdominal Hypertension / pathology
  • Intra-Abdominal Hypertension / surgery*
  • Laparotomy*
  • Liver / metabolism
  • Liver / pathology
  • Liver / physiopathology*
  • Rats
  • Rats, Sprague-Dawley
  • STAT3 Transcription Factor / metabolism
  • Sepsis / metabolism
  • Sepsis / pathology
  • Sepsis / surgery*
  • Suppressor of Cytokine Signaling Proteins / metabolism
  • Toll-Like Receptor 4 / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Interleukin-6
  • SOCS6 protein, rat
  • STAT3 Transcription Factor
  • Stat3 protein, rat
  • Suppressor of Cytokine Signaling Proteins
  • Tlr4 protein, rat
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha