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J Appl Physiol (February 2, 2006). doi:10.1152/japplphysiol.01439.2005
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Submitted on November 15, 2005
Accepted on January 25, 2006

SNORING-RELATED ENERGY TRANSMISSION TO THE CAROTID ARTERY IN RABBITS

Jason Amatoury1*, Lauren Howitt2, John R. Wheatley3, Albert P. Avolio4, and Terence C. Amis3

1 Ludwig Engel Centre for Respiratory Research, Westmead Hospital, Sydney, NSW, Australia; Graduate School of Biomedical Engineering, University of New South Wales, Sydney, NSW, Australia
2 Ludwig Engel Centre for Respiratory Research, Westmead Hospital, Sydney, NSW, Australia
3 Ludwig Engel Centre for Respiratory Research, Westmead Hospital, Sydney, NSW, Australia; Faculty of Medicine, University of Sydney, Sydney, NSW, Australia
4 Graduate School of Biomedical Engineering, University of New South Wales, Sydney, NSW, Australia

* To whom correspondence should be addressed. E-mail: jasonam{at}westgate.wh.usyd.edu.au.

Epidemiological studies link habitual snoring and stroke but mechanisms involved are poorly understood. One previously advanced hypothesis is that transmitted snoring vibration energy may promote carotid atheromatous plaque formation or rupture. In order to test whether vibration energy is present in carotid artery walls during snoring we developed an animal model in which we examined induced snoring (IS) associated tissue energy levels. Methods: In 6 male, supine, anaesthetised, spontaneously breathing, New Zealand White rabbits, we surgically inserted pressure transducer-tipped catheters (Millar) to monitor tissue pressure at the carotid artery bifurcation (pCT) and within the carotid sinus lumen (pCS; artery ligated). Snoring was induced via external compression (sandbag) over the pharyngeal region. Data were analysed using power spectral analysis for frequency bands above and below 50 Hz. Results: For frequencies below 50 Hz, pCT energy was 2.2(1.1-12.3) cmH2O2 (median(IQR)) during tidal breathing (TB) increasing to 39.0(2.5-95.0) cmH2O2 during IS (P = 0.05, Wilcoxon Signed Rank Test). For frequencies > 50 Hz, pCT energy increased from 9.2(8.3-10.4)x10-4 cmH2O2 during TB to 172.0(118.0-569.0)x10-4 cmH2O2 during IS (P = 0.03). Concurrently, pCS energy was 13.4(8.5-18.0)x10-4 cmH2O2 during TB and 151.0(78.2-278.8)x10-4 cmH2O2 during IS (P < 0.03). The pCS energy was greater than pCT energy for the 100-275 Hz bandwidth. Conclusions: During IS there is increased energy around and within the carotid artery, including lower frequency amplification for pCS. These findings may have implications for carotid atherogenesis and/or plaque rupture.




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