Vibration-induced vascular injury

Prolonged exposure to hand transmitted vibration can cause debilitating vascular dysfunctions in humans. Knowledge of the cell types damaged and the mechanisms of injury following acute vibration is critical for preventing incapacitating vascular injury. Details at the cellular level are lacking in part due to the absence of an animal model. The present research was designed to (1) develop an animal model for investigating the acute effects of vibration on arteries, (2) utilize this model to examine the role of frequency and amplitude in vascular damage, and (3) evaluate preventative measures. Selectively vibrating a rat's tail 4 hr/day for 1, 3, or 9 days at continuous 30,60, 120 and 800 Hz vibration (49 m/s2) with the remainder of the animal at rest proved well suited for assessing vascular damage. Vibrated, sham-vibrated, and normal arteries were processed for light and electron microscopy. One 4 hr, 60 Hz, 49 m/s2 treatment produced necrosis in a subpopulation of endothelial cells. Injury was signaled by elevated immunostaining for NFATc3 transcription factor and confirmed morphologically with electron microscopy. After 9 days of vibration, electron microscopy revealed thinning of endothelial cells with activated platelets coating the exposed subendothelial tissue and regions of denuded endothelium. Smooth muscle cells transformed from a contractile to a secretory phenotype. Endothelial cells and arterial smooth muscle cells contained double membrane-limited, swollen processes indicative of vasoconstriction-induced damage. Laser Doppler recording demonstrated that 5 min of vibration significantly diminished tissue blood perfusion, suggesting vibration-induced vasoconstriction. Pg. 9 Single 4 hr bouts of continuous 30, 60, 120 and 800 Hz vibration (49 m/s2) on the rat-tail artery were imposed to assess frequency- and amplitude-related damage. Amplitudes were 4.0, 0.9, 0.25 and 0.006 mm, respectively. 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 cellular vacuolization, indicative of vasoconstriction, occurred for all frequencies except 800 Hz. Vacuoles increased in endothelial and smooth muscle cells after 60 and 120 Hz. Only 30 Hz showed pronounced smooth muscle cell vacuolization at the internal and external elastic membranes. Vibration increased discontinuities, putative weakened sites, in the internal elastic membranes. Missing internal elastic membranes and overlying endothelium occurred in ∼5% of arteries after 60, 120 and 800 Hz, but not 30 Hz. It was concluded that vibration-induced vasoconstriction is frequency dependent (60 Hz = 120 Hz > 30 Hz).; Administration of the Ca++ channel blocker nifedipine 4 hrs prior to 60 Hz, 49 m/s2 vibration produced vasodilated arterial lumens compared to non-medicated sham-controls and prevented formation of smooth muscle vacuoles. Epinephrine (and norepinephrine), applied in situ to a surgically exposed ventral tail artery, and vibration both generated double membrane-limited vacuoles in the tunica media that was not observed in sham-vibrated arteries. Together, these results suggest that blockage of vibration-induced vasoconstriction prevents acute endothelial and smooth muscle cell damage. (Abstract shortened by UMI.)...