PMID- 25312742
OWN - NLM
STAT- MEDLINE
DCOM- 20150929
LR  - 20151119
IS  - 1399-6576 (Electronic)
IS  - 0001-5172 (Linking)
VI  - 59
IP  - 2
DP  - 2015 Feb
TI  - Effect of unfractionated heparin on endothelial glycocalyx in a septic shock 
      model.
PG  - 160-9
LID - 10.1111/aas.12418 [doi]
AB  - BACKGROUND: The constituents of vascular endothelial glycocalyx, such as 
      syndecan-1 and heparan sulphate (HS), can be detected in the plasma of patients 
      and animals with septic shock. However, the dynamics of glycocalyx degradation 
      and its association with inflammation remains largely unknown. In this study, we 
      investigated the association between the biomarkers of acute endothelial 
      glycocalyx degradation and inflammatory factors. We also evaluated the effect of 
      unfractionated heparin (UFH) on glycocalyx shedding in a canine septic shock 
      model. METHODS: Twenty adult beagle dogs were randomly allocated to one of the 
      following four groups (n = 5): (1) a sham group; (2) a shock group [3.5 x 10(8) 
      colony-forming unit (cfu) Escherichia coli (E. coli)/kg]; (3) a basic therapy 
      group (sensitive antibiotics and 0.9% saline, 10 ml/kg/h); and (4) a heparin 
      group (40 units/kg/h UFH plus basic therapy). After the onset of septic shock, 
      systemic haemodynamic indices were measured. Endothelial glycocalyx degradation 
      markers (i.e., syndecan-1, HS) and inflammatory factors [i.e., interleukin 6 
      (IL-6), tumour necrosis factor (TNF)-alpha], platelet count and activated partial 
      thromboplastin time were measured at various time points. RESULTS: A lethal dose 
      of E. coli induced a progressive septic shock model. We observed increased 
      syndecan-1 and HS levels, which correlated with IL-6 and TNF-alpha in the septic 
      shock model. The glycocalyx shedding was reduced by UFH, which might be regulated 
      by the inhibition of inflammatory factors. CONCLUSIONS: A therapeutic dose of UFH 
      can protect glycocalyx from shedding by inhibiting inflammation. Additional 
      studies with larger sample sizes are needed to confirm our conclusions.
CI  - (c) 2014 The Acta Anaesthesiologica Scandinavica Foundation. Published by John 
      Wiley & Sons Ltd.
FAU - Yini, S
AU  - Yini S
AD  - Department of Intensive Care Unit, The First Affiliated Hospital of China Medical 
      University, Shenyang, China.
FAU - Heng, Z
AU  - Heng Z
FAU - Xin, A
AU  - Xin A
FAU - Xiaochun, M
AU  - Xiaochun M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141014
PL  - England
TA  - Acta Anaesthesiol Scand
JT  - Acta anaesthesiologica Scandinavica
JID - 0370270
RN  - 0 (Biomarkers)
RN  - 0 (Fibrinolytic Agents)
RN  - 0 (Interleukin-6)
RN  - 0 (Syndecan-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9005-49-6 (Heparin)
SB  - IM
CIN - Acta Anaesthesiol Scand. 2015 Feb;59(2):137-9. PMID: 25597986
MH  - Animals
MH  - Biomarkers/blood
MH  - Disease Models, Animal
MH  - Dogs
MH  - Endothelium, Vascular/*drug effects
MH  - Female
MH  - Fibrinolytic Agents/blood/*pharmacology
MH  - Glycocalyx/*drug effects
MH  - Heparin/blood/*pharmacology
MH  - Inflammation/blood
MH  - Interleukin-6/blood
MH  - Male
MH  - Partial Thromboplastin Time/statistics & numerical data
MH  - Platelet Count/statistics & numerical data
MH  - Shock, Septic/*blood
MH  - Syndecan-1/blood
MH  - Tumor Necrosis Factor-alpha/blood/drug effects
EDAT- 2014/10/15 06:00
MHDA- 2015/09/30 06:00
CRDT- 2014/10/15 06:00
PHST- 2014/08/27 00:00 [received]
PHST- 2014/08/28 00:00 [accepted]
PHST- 2014/10/15 06:00 [entrez]
PHST- 2014/10/15 06:00 [pubmed]
PHST- 2015/09/30 06:00 [medline]
AID - 10.1111/aas.12418 [doi]
PST - ppublish
SO  - Acta Anaesthesiol Scand. 2015 Feb;59(2):160-9. doi: 10.1111/aas.12418. Epub 2014 
      Oct 14.