PMID- 20336357
OWN - NLM
STAT- MEDLINE
DCOM- 20110427
LR  - 20211020
IS  - 1573-2576 (Electronic)
IS  - 0360-3997 (Linking)
VI  - 34
IP  - 1
DP  - 2011 Feb
TI  - Electrical vagus nerve stimulation and nicotine effects in peritonitis-induced 
      acute lung injury in rats.
PG  - 29-35
LID - 10.1007/s10753-010-9204-5 [doi]
AB  - The cholinergic anti-inflammatory pathway has been identified as playing a key 
      role in the communication between the central nervous system and the immune 
      system during inflammation. The potential beneficial role of vagus nerve 
      stimulation (VNS) remains to be clarified in established sepsis. We hypothesized 
      that VNS or nicotine administration would reduce lung injury and mortality in 
      established sepsis. We conducted a prospective, randomized experimental study. 
      Four hours after peritonitis induction by cecal ligation and puncture (CLP), rats 
      were randomized into three groups of seven animals according to the intervention: 
      control group, VNS group (15 V, 2 ms, 5 Hz during 20 min), and nicotine group 
      (400 microg/kg intraperitoneal). Survival was determined as lung injury score 4 and 
      8 h after CLP. Tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-10, 
      cytokine-induced neutrophil chemoattractant (CINC)-3 and thrombin-antithrombin 
      complexes (TATc) were measured at baseline and at 4 and 8 h after CLP. Survival 
      at 8 h was 71.4%, 100%, and 23.8% in the control, VNS, and nicotine groups, 
      respectively (p < 0.05). All animals had lung damage but without significant 
      difference between groups even if nicotine-treated animals tended to have a 
      higher score than the controls (p = 0.09). Neutrophil polymorphonuclear (PMN) 
      infiltration was more pronounced in the nicotine group compared with the VNS 
      group (p = 0.015) but not with the controls. TNF-alpha, IL-6, IL-10, CINC-3, and TATc 
      were elevated in all groups (NS). In this model of established sepsis, 
      posttreatment by VNS was associated with increased survival, while nicotine 
      administration increased lung PMN infiltration and mortality. Nicotine-induced 
      bacterial clearance impairment and nicotine systemic effects may explain these 
      observations.
FAU - Boland, Claire
AU  - Boland C
AD  - Department of Critical Care Medicine, Saint-Luc University Hospital, Universite 
      Catholique de Louvain, Brussels, Belgium.
FAU - Collet, Valerie
AU  - Collet V
FAU - Laterre, Emmanuelle
AU  - Laterre E
FAU - Lecuivre, Corinne
AU  - Lecuivre C
FAU - Wittebole, Xavier
AU  - Wittebole X
FAU - Laterre, Pierre-Francois
AU  - Laterre PF
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (Chemokine CXCL2)
RN  - 0 (Cxcl2 protein, rat)
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (antithrombin III-protease complex)
RN  - 130068-27-8 (Interleukin-10)
RN  - 6M3C89ZY6R (Nicotine)
RN  - 9000-94-6 (Antithrombin III)
RN  - EC 3.4.- (Peptide Hydrolases)
SB  - IM
MH  - Acute Lung Injury/*immunology/*pathology
MH  - Animals
MH  - Antithrombin III
MH  - Cecum
MH  - Chemokine CXCL2/blood
MH  - *Electric Stimulation Therapy
MH  - Inflammation/immunology
MH  - Interleukin-10/blood
MH  - Interleukin-6/blood
MH  - Kaplan-Meier Estimate
MH  - Ligation
MH  - Neutrophil Infiltration/drug effects
MH  - Nicotine/*pharmacology
MH  - Peptide Hydrolases/blood
MH  - Peritonitis/complications/*immunology/*pathology
MH  - Rats
MH  - Tumor Necrosis Factor-alpha/blood
MH  - Vagus Nerve/*physiology
EDAT- 2010/03/26 06:00
MHDA- 2011/04/28 06:00
CRDT- 2010/03/26 06:00
PHST- 2010/03/26 06:00 [entrez]
PHST- 2010/03/26 06:00 [pubmed]
PHST- 2011/04/28 06:00 [medline]
AID - 10.1007/s10753-010-9204-5 [doi]
PST - ppublish
SO  - Inflammation. 2011 Feb;34(1):29-35. doi: 10.1007/s10753-010-9204-5.