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Fractal rigidity by enhanced sympatho-vagal antagonism in heartbeat interval dynamics elicited by central application of corticotropin-releasing factor in mice

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Meyer,  Michael
Fractal physiology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Stiedl,  Oliver
Molecular neuroendocrinology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Citation

Meyer, M., & Stiedl, O. (2006). Fractal rigidity by enhanced sympatho-vagal antagonism in heartbeat interval dynamics elicited by central application of corticotropin-releasing factor in mice. Journal of Mathematical Biology, 52(6), 830-874. doi:10.1007/s00285-006-0375-5.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002A-245A-6
Abstract
The dynamics of heartbeat interval fluctuations were studied in awake unrestrained mice following intracerebroventricular application of the neuropeptide corticotropin-releasing factor (CRF). The cardiac time series derived from telemetric ECG monitoring were analyzed by non-parametric techniques of nonlinear signal processing: delay-vector variance (DVV) analysis, higher-order variability (HOV) analysis, empirical mode decomposition (EMD), multiscale embedding-space decomposition (MESD), multiexponent multifractal (MEMF) analysis. The analyses support the conjecture that cardiac dynamics of normal control mice has both deterministic and stochastic elements, is nonstationary, nonlinear, and exerts multifractal properties. Central application of CRF results in bradycardia and increased variability of the beat-to-beat fluctuations. The altered dynamical properties elicited by CRF reflect a significant loss of intrinsic structural complexity of cardiac control which is due to central neuroautonomic hyperexcitation, i.e., enhanced sympatho-vagal antagonism. The change in dynamical complexity is characterized by an effect referred to as fractal rigidity, leading to a significant impairment of adaptability to extrinsic challenges in a fluctuating environment. The impact of dynamical neurocardiopathy as a major precipiting factor for the propensity of cardiac arrhythmias or sudden cardiac death by unchecked central CRF release in significant acute life events in man is critically discussed.