title: Evidence for frequency-dependent arterial damage in vibrated rat tails.
abstract: The effects of single 4-hr bouts of continuous 30, 60, 120, and 800 Hz tail vibration (49 m/sec2, root mean squared) were compared to assess frequency-amplitude-related structural damage of the ventral caudal artery. Amplitudes were 3.9, 0.98, 0.24, and 0.0055 mm, respectively. Vibrated, sham-vibrated, and normal arteries were processed for light and electron microscopy. The Curry rat tail model of hand-arm vibration (Curry et al. Muscle Nerve 2002;25:527-534) proved well-suited for testing multiple frequencies. NFATc3 immunostaining, an early marker of cell damage, increased in smooth muscle and endothelial cells after 30, 60, and 120 Hz but not 800 Hz. Increased vacuolization, which is indicative of smooth muscle contraction, occurred for all frequencies except 800 Hz. Vacuoles increased in both endothelial and smooth muscle cells after 60 and 120 Hz. Only 30 Hz showed pronounced smooth muscle cell vacuolization along the internal and external elastic membranes, suggesting stretch-mediated contraction from the large amplitude shear stress. Discontinuities in toluidine blue staining of the internal elastic membrane (IEM) increased for all frequencies, indicating vibration-induced structural weakening of this structure. Patches of missing IEM and overlying endothelium occurred in approximately 5% of arteries after 60, 120, and 800 Hz. The pattern of damage after 800 Hz suggests that the IEM is disrupted because it resonates at this frequency. Vibration acceleration stress and smooth muscle contraction appear to be the major contributors to arterial damage. The pattern of vibration-induced arterial damage of smooth muscle and endothelial cells is frequency-amplitude-dependent.
authors.affiliation: Department of Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
authors.forename: Brian D
authors.initials: BD
authors.lastname: Curry
authors.forename: Sandya R
authors.initials: SR
authors.lastname: Govindaraju
authors.forename: James L W
authors.initials: JL
authors.lastname: Bain
authors.forename: Lin Ling
authors.initials: LL
authors.lastname: Zhang
authors.forename: Ji-Geng
authors.initials: JG
authors.lastname: Yan
authors.forename: Hani S
authors.initials: HS
authors.lastname: Matloub
authors.forename: Danny A
authors.initials: DA
authors.lastname: Riley
mesh_terms: D000818:Animals; D001158:Arteries / Q000293:injuries* / Q000473:pathology* / Q000648:ultrastructure; D004268:DNA-Binding Proteins / Q000378:metabolism; D004730:Endothelium, Vascular / Q000293:injuries* / Q000473:pathology* / Q000648:ultrastructure; D007150:Immunohistochemistry; D008297:Male; D050778:NFATC Transcription Factors; D009784:Occupational Diseases / Q000209:etiology* / Q000473:pathology*; D010812:Physical Stimulation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow / Q000502:physiology; D012149:Restraint, Physical / Q000523:psychology; D013623:Tail / Q000098:blood supply / Q000293:injuries / Q000473:pathology; D014157:Transcription Factors / Q000378:metabolism; D014732:Vibration / Q000009:adverse effects*
chemical_list: D004268:DNA-Binding Proteins; D050778:NFATC Transcription Factors; D014157:Transcription Factors; C445503:transcription factor NF-AT c3