PMID- 26276818
OWN - NLM
STAT- MEDLINE
DCOM- 20151229
LR  - 20200930
IS  - 1522-1539 (Electronic)
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 309
IP  - 7
DP  - 2015 Oct
TI  - Vagus nerve stimulation mitigates intrinsic cardiac neuronal and adverse myocyte 
      remodeling postmyocardial infarction.
PG  - H1198-206
LID - 10.1152/ajpheart.00393.2015 [doi]
AB  - This paper aims to determine whether chronic vagus nerve stimulation (VNS) 
      mitigates myocardial infarction (MI)-induced remodeling of the intrinsic cardiac 
      nervous system (ICNS), along with the cardiac tissue it regulates. Guinea pigs 
      underwent VNS implantation on the right cervical vagus. Two weeks later, MI was 
      produced by ligating the ventral descending coronary artery. VNS stimulation 
      started 7 days post-MI (20 Hz, 0.9 +/- 0.2 mA, 14 s on, 48 s off; VNS-MI, n = 7) 
      and was compared with time-matched MI animals with sham VNS (MI n = 7) vs. 
      untreated controls (n = 8). Echocardiograms were performed before and at 90 days 
      post-MI. At termination, IC neuronal intracellular voltage recordings were 
      obtained from whole-mount neuronal plexuses. MI increased left ventricular end 
      systolic volume (LVESV) 30% (P = 0.027) and reduced LV ejection fraction (LVEF) 
      6.5% (P < 0.001) at 90 days post-MI compared with baseline. In the VNS-MI group, 
      LVESV and LVEF did not differ from baseline. IC neurons showed depolarization of 
      resting membrane potentials and increased input resistance in MI compared with 
      VNS-MI and sham controls (P < 0.05). Neuronal excitability and sensitivity to 
      norepinephrine increased in MI and VNS-MI groups compared with controls (P < 
      0.05). Synaptic efficacy, as determined by evoked responses to stimulating input 
      axons, was reduced in VNS-MI compared with MI or controls (P < 0.05). VNS induced 
      changes in myocytes, consistent with enhanced glycogenolysis, and blunted the 
      MI-induced increase in the proapoptotic Bcl-2-associated X protein (P < 0.05). 
      VNS mitigates MI-induced remodeling of the ICNS, correspondingly preserving 
      ventricular function via both neural and cardiomyocyte-dependent actions.
CI  - Copyright (c) 2015 the American Physiological Society.
FAU - Beaumont, Eric
AU  - Beaumont E
AD  - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee 
      State University, Johnson City, Tennessee;
FAU - Southerland, Elizabeth M
AU  - Southerland EM
AD  - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee 
      State University, Johnson City, Tennessee;
FAU - Hardwick, Jean C
AU  - Hardwick JC
AD  - Department of Biology, Ithaca College, Ithaca, New York;
FAU - Wright, Gary L
AU  - Wright GL
AD  - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee 
      State University, Johnson City, Tennessee;
FAU - Ryan, Shannon
AU  - Ryan S
AD  - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee 
      State University, Johnson City, Tennessee;
FAU - Li, Ying
AU  - Li Y
AD  - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee 
      State University, Johnson City, Tennessee;
FAU - KenKnight, Bruce H
AU  - KenKnight BH
AD  - Cyberonics, Houston, Texas; and.
FAU - Armour, J Andrew
AU  - Armour JA
AD  - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee 
      State University, Johnson City, Tennessee; Department of Medicine, University of 
      California Los Angeles Health System, Los Angeles, California.
FAU - Ardell, Jeffrey L
AU  - Ardell JL
AD  - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee 
      State University, Johnson City, Tennessee; Department of Medicine, University of 
      California Los Angeles Health System, Los Angeles, California 
      jardell@mednet.ucla.edu.
LA  - eng
GR  - HL09889/HL/NHLBI NIH HHS/United States
GR  - HL71830/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20150814
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (bcl-2-Associated X Protein)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Animals
MH  - Autonomic Nervous System/*physiopathology
MH  - Evoked Potentials
MH  - Glycogenolysis
MH  - Guinea Pigs
MH  - Heart/*innervation
MH  - Membrane Potentials
MH  - Myocardial Infarction/*physiopathology
MH  - Myocytes, Cardiac/*metabolism
MH  - Neuronal Plasticity/*physiology
MH  - Norepinephrine/metabolism
MH  - Stroke Volume/physiology
MH  - Synaptic Transmission
MH  - *Vagus Nerve Stimulation
MH  - Ventricular Dysfunction, Left/*physiopathology
MH  - Ventricular Function, Left
MH  - bcl-2-Associated X Protein/metabolism
PMC - PMC4666924
OTO - NOTNLM
OT  - autonomic regulation therapy
OT  - guinea pig
OT  - intrinsic cardiac nervous system
OT  - myocardial infarction
OT  - vagus nerve stimulation
EDAT- 2015/08/16 06:00
MHDA- 2015/12/30 06:00
PMCR- 2016/10/01
CRDT- 2015/08/16 06:00
PHST- 2015/05/27 00:00 [received]
PHST- 2015/08/10 00:00 [accepted]
PHST- 2015/08/16 06:00 [entrez]
PHST- 2015/08/16 06:00 [pubmed]
PHST- 2015/12/30 06:00 [medline]
PHST- 2016/10/01 00:00 [pmc-release]
AID - ajpheart.00393.2015 [pii]
AID - H-00393-2015 [pii]
AID - 10.1152/ajpheart.00393.2015 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2015 Oct;309(7):H1198-206. doi: 
      10.1152/ajpheart.00393.2015. Epub 2015 Aug 14.