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- Josef Gehrmann
- Department of Cardiology, Children's Hospital-Boston, and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
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- Peter E. Hammer
- Department of Cardiology, Children's Hospital-Boston, and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
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- Colin T. Maguire
- Department of Cardiology, Children's Hospital-Boston, and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
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- Hiroko Wakimoto
- Department of Cardiology, Children's Hospital-Boston, and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
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- John K. Triedman
- Department of Cardiology, Children's Hospital-Boston, and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
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- Charles I. Berul
- Department of Cardiology, Children's Hospital-Boston, and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
説明
<jats:p> We developed a technology for heart rate (HR) variability (HRV) analysis in the mouse for characterization of HR dynamics, modulated by vagal and sympathetic activity. The mouse is the principal animal model for studying biological processes. Mouse strains are now available harboring gene mutations providing fundamental insights into molecular mechanisms underlying cardiac electrical diseases. Future progress depends on enhanced understanding of these fundamental mechanisms and the implementation of methods for the functional analysis of mouse cardiovascular physiology. By telemetric techniques, standard time and frequency-domain measures of HRV were computed with and without autonomic blockade, and baroreflex sensitivity testing was performed. HR modulation in the high-frequency component is predominantly mediated by the parasympathetic nervous system, whereas the low-frequency component is under the influence of both the parasympathetic and sympathetic systems. The presented technology and protocol allow for assessment of autonomic regulation of the murine HR. Phenotypic screening for HR regulation in mice will further enhance the value of the mouse as a model of heritable electrophysiological human disease. </jats:p>
収録刊行物
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- American Journal of Physiology-Heart and Circulatory Physiology
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American Journal of Physiology-Heart and Circulatory Physiology 279 (2), H733-H740, 2000-08-01
American Physiological Society
