PMID- 27798536
OWN - NLM
STAT- MEDLINE
DCOM- 20170627
LR  - 20181202
IS  - 1540-0514 (Electronic)
IS  - 1073-2322 (Linking)
VI  - 47
IP  - 5
DP  - 2017 May
TI  - Influences of Vagotomy on Gut Ischemia-Reperfusion Injury in Mice.
PG  - 646-652
LID - 10.1097/SHK.0000000000000783 [doi]
AB  - BACKGROUND: How vagotomy affects host responses to gut ischemia-reperfusion (I/R) 
      is unclear. MATERIALS AND METHODS: Experiment 1: male Institute of Cancer 
      Research mice (n = 22) were assigned to the I/R or the vago-I/R group. The I/R 
      mice underwent 45-min superior mesenteric artery (SMA) occlusion. The vago-I/R 
      mice received vagotomy before SMA occlusion. Survival was observed for 
      48 h.Experiment 2: mice (n = 55) were divided into four groups (Sham, vago, I/R, 
      vago-I/R). Sham and vago groups did not undergo gut I/R. Mice were killed at 3 or 
      6 h after reperfusion, and cytokine levels in the plasma, jejunum, and ileum were 
      evaluated. In addition, gut histology at 6 h was examined.Experiment 3: mice 
      (n = 24) were divided into four groups as in Experiment 2. The small intestine 
      was harvested at 3 h after reperfusion and the tissue was cultured ex vivo for 
      3 h. Cytokine levels of the culture supernatant were then measured. RESULTS: 
      Experiment 1: survival was significantly worse with vago-I/R than I/R.Experiment 
      2: along with severe gut injury, vago-I/R increased IL-6 and monocyte 
      chemoattractant protein-1 (MCP-1) in plasma, IFN-gamma in the jejunum and MCP-1 in 
      the ileum, as compared with I/R. Significant positive correlations were noted 
      between plasma and intestinal levels of pro-inflammatory cytokines (IL-6, MCP-1, 
      and TNF-alpha).Experiment 3: MCP-1 in the jejunal culture medium was higher in the 
      vago-I/R than in the I/R group. CONCLUSIONS: Vagotomy worsens survival after gut 
      I/R, together with increases in pro-inflammatory cytokines in both plasma and the 
      gut in association with severe intestinal tissue damage.
FAU - Ri, Motonari
AU  - Ri M
AD  - *Department of Gastrointestinal Surgery, Graduate School of Medicine, The 
      University of Tokyo, Tokyo, Japan daggerDepartment of Surgical Center, The University 
      of Tokyo, Tokyo, Japan double daggerDepartment of Digestive Surgery, Nihon University School 
      of Medicine, Tokyo, Japan  section signDepartment of Laboratory of Veterinary Surgery, The 
      University of Tokyo, Tokyo, Japan.
FAU - Fukatsu, Kazuhiko
AU  - Fukatsu K
FAU - Miyakuni, Taiki
AU  - Miyakuni T
FAU - Yanagawa, Masashi
AU  - Yanagawa M
FAU - Murakoshi, Satoshi
AU  - Murakoshi S
FAU - Yasuhara, Hiroshi
AU  - Yasuhara H
FAU - Seto, Yasuyuki
AU  - Seto Y
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/blood/metabolism
MH  - Cytokines/blood/metabolism
MH  - Ileum/metabolism
MH  - Interleukin-6/blood/metabolism
MH  - Intestinal Mucosa/*metabolism
MH  - Intestine, Small/metabolism
MH  - Intestines/injuries
MH  - Ischemia/*immunology/mortality
MH  - Male
MH  - Mice
MH  - Reperfusion Injury/*immunology/mortality
MH  - Tumor Necrosis Factor-alpha/blood/metabolism
MH  - Vagotomy/*adverse effects
MH  - Vagus Nerve/metabolism/surgery
EDAT- 2016/11/01 06:00
MHDA- 2017/06/28 06:00
CRDT- 2016/11/01 06:00
PHST- 2016/11/01 06:00 [pubmed]
PHST- 2017/06/28 06:00 [medline]
PHST- 2016/11/01 06:00 [entrez]
AID - 10.1097/SHK.0000000000000783 [doi]
PST - ppublish
SO  - Shock. 2017 May;47(5):646-652. doi: 10.1097/SHK.0000000000000783.