Sandya Govindaraju

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/s2. 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. Muscle Nerve, 2006

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°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. Muscle Nerve, 2006

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/s2 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. Muscle Nerve, 2005