Snoring-related energy transmission to the carotid artery in rabbits

Snoring-related energy transmission to the carotid artery in rabbits. J Appl Physiol 100: 1547-1553, 2006. First published February 2, 2006; doi: 10.1152/japplphysiol. 01439.2005.- 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. 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. In six male, supine, anesthetized, 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 analyzed using power spectral analysis for frequency bands above and below 50 Hz. For frequencies below 50 Hz, PCT energy was 2.2 (1.1-12.3) cmH(2)O(2) [median (interquartile range)] during tidal breathing ( TB) increasing to 39.0 (2.5-95.0) cmH(2)O(2) during IS (P = 0.05, Wilcoxon's signed-rank test). For frequencies > 50 Hz, PCT energy increased from 9.2 (8.3-10.4) x 10(-4) cmH(2)O(2) during TB to 172.0 (118.0 - 569.0) x 10(-4) cmH(2)O(2) during IS (P = 0.03). Concurrently, PCS energy was 13.4 (8.5 - 18.0) x 10(-4) cmH(2)O(2) during TB and 151.0 (78.2-278.8) x 10(-4) cmH(2)O(2) during IS (P < 0.03). The PCS energy was greater than PCT energy for the 100 - 275 Hz bandwidth. In conclusion, 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.