Comparison of continuous and intermittent vibration effects on rat-tail artery and nerve.

Hand-transmitted vibration from powered-tools can cause peripheral vasospasm and neuropathy. A rat-tail model was used to investigate whether the pattern of vibration influenced the type and severity of tissue damage. The tails of awake rats were vibrated continuously or intermittently for a total of 4 hours at 60 HZ, 49 m/s(2). Nerves and arteries were harvested immediately or 24 hours after treatment. Tails subjected to intermittent vibration showed transiently increased sensitivity to thermal stimuli. Intermittent vibration caused the most nerve injury immediately and 24 hours after vibration. Continuous vibration invoked a persistent reduction in vascular lumen size. Compared to epinephrine-induced transient vacuolation in vascular smooth muscle cells, both continuous and intermittent vibration caused greater persistence of vacuoles, indicating a vibration-induced pathological process. All vibration groups exhibited elevated nitrotyrosine immunoreactivity indicative of free-radical damage. Pattern of vibration exposure may exert a major influence on the type of vibration injury.

Effects of temperature on vibration-induced damage in nerves and arteries.

Vasospastic episodes in hand-arm vibration syndrome are more prevalent among power-tool workers in cold climates. To test whether cold enhances vibration-induced damage in arteries and nerves, tails of Sprague-Dawley rats were vibrated at room temperature (RT) or with tail cooling (<15 degrees C). Cold vibration resulted in a colder tail than either treatment alone. Vibration at both temperatures reduced arterial lumen size. RT vibration generated more vacuoles in arteries than cold vibration. Vibration and cold induced nitration of tyrosine residues in arteries, suggesting free-radical production. Vibration and cold generated similar percentages of myelinated axons with disrupted myelin. Cold with and without vibration caused intraneural edema and dilation of arterioles and venules with blood stasis, whereas vibration alone did not. The similarities, differences, and interactive effects of cold and vibration on nerve and artery damage indicate that temperature is involved mechanistically in the pathophysiology of hand-arm vibration syndrome.

Nifedipine pretreatment reduces vibration-induced vascular damage.

A rat-tail vibration model of hand-arm vibration was employed to test whether preemptive administration of nifedipine (5 mg/kg) to block vasoconstriction prevents vibration-induced arterial damage. The tails of vibrated and nifedipine-pretreated vibrated Sprague-Dawley rats were exposed continuously to 4 h of 60-HZ vibration at 49 m/s(2) rms. In nonvibrated anesthetized rats, the ventral tail arteries were bathed for 15 min in situ in 1 mM epinephrine or 1 mM norepinephrine to induce structural changes indicative of intense vasoconstriction. Arteries were processed for light and electron microscopy 45 min after treatment. Compared to sham control, 4-h vibration significantly (P < 0.01) reduced lumen size, generated endothelial disruption (7.0 +/- 2.6%), elevated nuclear factor of activated T cells c3 (NFATc3) expression in endothelial and smooth muscle cells, and increased smooth muscle cell vacuolization. The findings demonstrate that blockage of vibration-induced vasoconstriction with nifedipine prevents acute vascular damage. Smooth muscle and endothelial cells structurally altered by vasoconstriction are rendered susceptible to damage by vibration.

Evidence for frequency-dependent arterial damage in vibrated rat tails.

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.

Vibration injury damages arterial endothelial cells.

Prolonged exposure to hand-transmitted vibration can cause debilitating neural and vascular dysfunction in humans. It is unclear whether the pathophysiology involves simultaneous or sequential injury of arteries and nerves. The mechanism of vibration injury was investigated in a rat tail model, containing arteries and nerves structurally similar to those in the human hand. Tails were selectively vibrated for 1 or 9 days with the remainder of the animal at rest. One vibration bout of 4 h/day, 60 HZ, 5 g (49 m/s(2)) acceleration, injured endothelial cells. Injury was signaled by elevated immunostaining for NFATc3 transcription factor. Electron microscopy revealed that vibration for 9 days produced loss and thinning of endothelial cells, with activated platelets coating the exposed subendothelial tissue. Endothelial cells and arterial smooth muscle cells contained double membrane-limited, swollen processes indicative of vasoconstriction-induced damage. Laser doppler surface recording demonstrated that 5 min of vibration significantly diminished tissue blood perfusion. These findings indicate that early injury involves vasoconstriction and denuding of the arterial endothelium.