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Articles in PresS, published online ahead of print January 10, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00600.2001
Submitted on July 10, 2001
Accepted on January 7, 2002
1 Psychiatry and the Behavioral Sciences, University of Southern California, Los Angeles, CA, USA; Neurology, University of Southern California, Los Angeles, CA, USA; Greater Los Angeles VA Healthcare System, Los Angeles, CA, USA
2 Greater Los Angeles VA Healthcare System, Los Angeles, CA, USA; Physiology, University of California at Los Angeles, Los Angeles, CA, USA
3 Molecular Pharmacology and Toxicology, University of Southern California, Los Angeles, CA, USA
4 Cell and Neurobiology, University of Southern California, Los Angeles, CA, USA; Molecular Pharmacology and Toxicology, University of Southern California, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: holschne{at}hsc.usc.edu.
Heart-rate dynamics were investigated in mice deficient in monoamine oxidase A and B, whose phenotype includes elevated tissue levels of norepinephrine, serotonin, dopamine and phenylethylamine. In their homecages, spectral analysis of the R-R intervals revealed more pronounced fluctuations at all frequencies in the mutants compared to wild-type controls, with a particular enhancement at 1-4 Hz. No significant genotypic differences in heart rate variability (HRV) or entropies calculated from Poincare plots of the R-R intervals were noted. During exposure to the stress of a novel environment, heart rates increased and HRV decreased in both genotypes. However, mutants unlike controls demonstrated a rapid return to baseline heart rates during the 10 minutes exposure. Such modulation may result from an enhanced vagal tone as suggested by the observation that mutants responded to cholinergic blockade with a decrease in HRV and a prolonged tachycardia greater than controls. Monoamine oxidase deficient mice may represent a useful experimental model for studying compensatory mechanisms responsible for changes in heart-rate dynamics in chronic states of high sympathetic tone.
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