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Intrathoracic neurons modify myocardial ischemia‐induced sudden cardiac death
Author(s) -
Ardell Jeffrey L,
Southerland E. Marie,
Armour J. Andrew
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.809.14
Subject(s) - medicine , microdialysis , ischemia , cardiology , sudden cardiac death , anesthesia , coronary occlusion , spinal cord , norepinephrine , central nervous system , dopamine , psychiatry
To determine if cardiac sympathetic intrathoracic reflexes represent a risk factor for ischemia‐induced sudden cardiac death (SCD) and, if so, whether targeting them reduces that risk. Left ventricular (LV) interstitial fluid (ISF) norepinephrine (NE) levels were assessed by microdialysis in anesthetized canines during transient coronary artery occlusion (CAO). Responses in animals with intact neuroaxes were compared to those in which the intrathoracic component of the cardiac neuronal hierarchy was surgically disconnected from central neurons vs those with intact neuroaxis that underwent spinal cord stimulation (SCS; T1‐T3 spinal level). In intact preparations, animals exhibiting enhanced NE ISF levels with increased dispersion between ischemic and border zone were at increased risk for SCD. Following intrathoracic neuronal decentralization, CAO induced NE release was reduced ~20% and uniform across the ischemic to border zones. Following intrinsic cardiac neuronal decentralization, CAO induced NE release occurred only in ischemic tissue. SCS also reduced CAO‐induced NE release (~60% vs control). Risk for CAO‐induced SCD was 42% in control, 8% following decentralization and 10% with SCS. These data demonstrate that stabilization of intrathoracic nervous system by such means reduces the potential for ischemia‐induced SCD while maintaining regulatory function. HL71830