TY - JOUR A1 - , T1 - Vascular lesions and vibroacoustic disease JO - Eur. J. Anat. SN - 1136-4890 Y1 - 2002 VL - 6 SP - 17 EP - 21 UR - http://www.eurjanat.com/web/paper.php?id=02010017 KW - animal experiment KW - animal model KW - animal tissue KW - aorta KW - artery diameter KW - artery intima proliferation KW - artery media KW - article KW - cell proliferation KW - controlled study KW - environmental exposure KW - extracellular matrix KW - femoral artery KW - hindlimb KW - histology KW - industrial noise KW - inferior cava vein KW - long term exposure KW - low frequency noise KW - noise injury KW - nonhuman KW - occupational exposure KW - pressure KW - rat KW - rat strain KW - simulation KW - smooth muscle fiber KW - thickness KW - vein KW - vibration KW - vibroacoustic disease N2 - Low frequency noise (LFN) (? 90 dB SPL, ? 500 Hz) is an agent of disease that regularly goes unchecked during standard noise assessment procedures. Vibroacoustic disease (VAD) is an extra-aural noise-induced systemic pathology, caused by long-term exposure to LFN and characterised by a proliferation of extra-cellular matrices. The present study attempts to elucidate the behaviour of medium-and large-calibre blood vessels in the presence of insult due to noise and vibration. Thirty-five adult Wistar rats were studied. The animals were divided into 3 groups. One group of 20 rats was exposed to large pressure amplitude and low frequency (LPALF) noise in an occupationally simulated schedule: 8 h/day, 5 days/week, and weekends in silence, for 968 to 1984 (median 1576 h) cumulative hours of noise exposure. Another group of 5 rats was exposed to 24 h of continuous noise. The last group of 10 rats (control) was kept under identical conditions but in a silent environment. Overall noise levels were recorded above 109 dB, the A-weighted levels being around 98 dB (A). The rats were sacrificed and fragments of aorta, inferior vena cava and femoral artery and vein from both hindlimbs, were collected; these were prepared for histological examination. With long-term exposure, the aorta and the femoral artery showed a focal thickening of the intima, disruption of the internal elastic lamina and a proliferation of smooth muscle cells in the intima in 70% of the cases. With acute exposure, the lesions appeared in 60% of the cases observed. Most of the lesions involved the appearance of clefts in the media, pulling the cells and the elastic membranes apart. The media thickness-to-inner caliber ratio of the femoral artery was increased (p<0.05). Our results point to a remodelling of the vessels that can be attributed to vibration and flow disturbances. The observed remodelling was not observed in small vessels. ER -