X J Du1, H S Cox, A M Dart, M D Esler. 1. Alfred and Baker Medical Unit, Baker Medical Research Institute, Melbourne, Victoria, Australia. xiaojun.du@baker.edu.au
Abstract
OBJECTIVE: To seek direct evidence for a cause-effect relation between sympathetic activation and arrhythmogenesis. METHODS: Rats underwent open-chest surgery with either coronary artery occlusion or sham operation, and were studied 8 weeks later using in situ heart perfusion and nerve stimulation methods. RESULTS: Infarcted rats showed cardiac functional impairment and increased heart and lung weight. The extent of these changes correlated well with infarct size (IS). In in situ perfused hearts, sympathetic nerve stimulation (2 and 4 Hz, 45 s duration) induced a frequency-dependent release of norepinephrine (NE). NE release was lower in MI than that in control groups. In hearts with large IS (> or = 40%, n = 19) ventricular arrhythmias were rare at baseline, but nerve stimulation evoked the onset of ventricular premature beats (95%), tachycardia (37%) and fibrillation (26%), IS and stimulation frequency were key determinants for the inducibility of arrhythmias. Lower K- concentration enhanced arrhythmia inducibility. beta-blockade inhibited the frequency of arrhythmias produced by nerve stimulation. CONCLUSION: In infarcted rat hearts sympathetic activation is a potent trigger for the onset of ventricular tachyarrhythmias.
OBJECTIVE: To seek direct evidence for a cause-effect relation between sympathetic activation and arrhythmogenesis. METHODS:Rats underwent open-chest surgery with either coronary artery occlusion or sham operation, and were studied 8 weeks later using in situ heart perfusion and nerve stimulation methods. RESULTS:Infarctedrats showed cardiac functional impairment and increased heart and lung weight. The extent of these changes correlated well with infarct size (IS). In in situ perfused hearts, sympathetic nerve stimulation (2 and 4 Hz, 45 s duration) induced a frequency-dependent release of norepinephrine (NE). NE release was lower in MI than that in control groups. In hearts with large IS (> or = 40%, n = 19) ventricular arrhythmias were rare at baseline, but nerve stimulation evoked the onset of ventricular premature beats (95%), tachycardia (37%) and fibrillation (26%), IS and stimulation frequency were key determinants for the inducibility of arrhythmias. Lower K- concentration enhanced arrhythmia inducibility. beta-blockade inhibited the frequency of arrhythmias produced by nerve stimulation. CONCLUSION: In infarctedrat hearts sympathetic activation is a potent trigger for the onset of ventricular tachyarrhythmias.
Authors: Diana C Parrish; Eric N Alston; Hermann Rohrer; Paul Nkadi; William R Woodward; Günther Schütz; Beth A Habecker Journal: Exp Physiol Date: 2009-10-30 Impact factor: 2.969
Authors: Christina U Lorentz; Diana C Parrish; Eric N Alston; Michael J Pellegrino; William R Woodward; Barbara L Hempstead; Beth A Habecker Journal: Exp Neurol Date: 2013-09-03 Impact factor: 5.330
Authors: Helen Kiriazis; Nicole L Jennings; Pamela Davern; Gavin Lambert; Yidan Su; Terence Pang; Xin Du; Luisa La Greca; Geoffrey A Head; Anthony J Hannan; Xiao-Jun Du Journal: J Physiol Date: 2012-08-13 Impact factor: 5.182
Authors: Samantha D Francis Stuart; Lianguo Wang; William R Woodard; G Andre Ng; Beth A Habecker; Crystal M Ripplinger Journal: J Physiol Date: 2018-08-03 Impact factor: 5.182