PMID- 27422985
OWN - NLM
STAT- MEDLINE
DCOM- 20170626
LR  - 20200930
IS  - 1522-1539 (Electronic)
IS  - 0363-6135 (Linking)
VI  - 311
IP  - 3
DP  - 2016 Sep 1
TI  - Partial IK1 blockade destabilizes spiral wave rotation center without inducing 
      wave breakup and facilitates termination of reentrant arrhythmias in ventricles.
PG  - H750-8
LID - 10.1152/ajpheart.00228.2016 [doi]
AB  - It has been reported that blockade of the inward rectifier K(+) current (IK1) 
      facilitates termination of ventricular fibrillation. We hypothesized that partial 
      IK1 blockade destabilizes spiral wave (SW) re-entry, leading to its termination. 
      Optical action potential (AP) signals were recorded from left ventricles of 
      Langendorff-perfused rabbit hearts with endocardial cryoablation. The dynamics of 
      SW re-entry were analyzed during ventricular tachycardia (VT), induced by 
      cross-field stimulation. Intercellular electrical coupling in the myocardial 
      tissue was evaluated by the space constant. In separate experiments, AP 
      recordings were made using the microelectrode technique from right ventricular 
      papillary muscles of rabbit hearts. Ba(2+) (10-50 muM) caused a dose-dependent 
      prolongation of VT cycle length and facilitated termination of VT in perfused 
      hearts. Baseline VT was maintained by a stable rotor, where an SW rotated around 
      an I-shaped functional block line (FBL). Ba(2+) at 10 muM prolonged I-shaped FBL 
      and phase-singularity trajectory, whereas Ba(2+) at 50 muM transformed the SW 
      rotation dynamics from a stable linear pattern to unstable circular/cycloidal 
      meandering. The SW destabilization was not accompanied by SW breakup. Under 
      constant pacing, Ba(2+) caused a dose-dependent prolongation of APs, and Ba(2+) 
      at 50 muM decreased conduction velocity. In papillary muscles, Ba(2+) at 50 muM 
      depolarized the resting membrane potential. The space constant was increased by 
      50 muM Ba(2+) Partial IK1 blockade destabilizes SW rotation dynamics through a 
      combination of prolongation of the wave length, reduction of excitability, and 
      enhancement of electrotonic interactions, which facilitates termination of 
      ventricular tachyarrhythmias.
CI  - Copyright (c) 2016 the American Physiological Society.
FAU - Kushiyama, Yasunori
AU  - Kushiyama Y
AD  - Department of Cardiovascular Research, Research Institute of Environmental 
      Medicine, Nagoya University, Nagoya, Japan; and.
FAU - Honjo, Haruo
AU  - Honjo H
AD  - Department of Cardiovascular Research, Research Institute of Environmental 
      Medicine, Nagoya University, Nagoya, Japan; and honjo@riem.nagoya-u.ac.jp.
FAU - Niwa, Ryoko
AU  - Niwa R
AD  - Department of Cardiovascular Research, Research Institute of Environmental 
      Medicine, Nagoya University, Nagoya, Japan; and.
FAU - Takanari, Hiroki
AU  - Takanari H
AD  - Department of Cardiovascular Research, Research Institute of Environmental 
      Medicine, Nagoya University, Nagoya, Japan; and.
FAU - Yamazaki, Masatoshi
AU  - Yamazaki M
AD  - Department of Cardiovascular Research, Research Institute of Environmental 
      Medicine, Nagoya University, Nagoya, Japan; and.
FAU - Takemoto, Yoshio
AU  - Takemoto Y
AD  - Department of Cardiovascular Research, Research Institute of Environmental 
      Medicine, Nagoya University, Nagoya, Japan; and.
FAU - Sakuma, Ichiro
AU  - Sakuma I
AD  - Graduate School of Engineering, The University of Tokyo, Tokyo, Japan.
FAU - Kodama, Itsuo
AU  - Kodama I
AD  - Department of Cardiovascular Research, Research Institute of Environmental 
      Medicine, Nagoya University, Nagoya, Japan; and.
FAU - Kamiya, Kaichiro
AU  - Kamiya K
AD  - Department of Cardiovascular Research, Research Institute of Environmental 
      Medicine, Nagoya University, Nagoya, Japan; and.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160715
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Potassium Channels, Inwardly Rectifying)
RN  - 24GP945V5T (Barium)
SB  - IM
MH  - Action Potentials/*drug effects
MH  - Animals
MH  - Arrhythmias, Cardiac
MH  - Barium/*pharmacology
MH  - Cryosurgery
MH  - Heart/*drug effects/physiopathology
MH  - Isolated Heart Preparation
MH  - Myocardium/*metabolism
MH  - Optical Imaging
MH  - Potassium Channels, Inwardly Rectifying/*antagonists & inhibitors/metabolism
MH  - Rabbits
MH  - Tachycardia, Ventricular/*metabolism/physiopathology
MH  - Ventricular Fibrillation/*metabolism/physiopathology
OTO - NOTNLM
OT  - inward rectifier K+ current
OT  - optical mapping
OT  - spiral wave re-entry
OT  - ventricular tachycardia
EDAT- 2016/07/17 06:00
MHDA- 2017/06/27 06:00
CRDT- 2016/07/17 06:00
PHST- 2016/03/11 00:00 [received]
PHST- 2016/07/13 00:00 [accepted]
PHST- 2016/07/17 06:00 [entrez]
PHST- 2016/07/17 06:00 [pubmed]
PHST- 2017/06/27 06:00 [medline]
AID - ajpheart.00228.2016 [pii]
AID - 10.1152/ajpheart.00228.2016 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2016 Sep 1;311(3):H750-8. doi: 
      10.1152/ajpheart.00228.2016. Epub 2016 Jul 15.