Nifedipine pretreatment reduces vibration‐induced vascular damage

Curry, Brian; Govindaraju, Sandya; Bain, James L. W.; Zhang, Lin Ling; Yan, Ji‐Geng; Matloub, Hani S.; Riley, Denise

doi:10.1002/mus.20388

Cited by 16 publications

(21 citation statements)

References 33 publications

(39 reference statements)

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“…26 In the rat-tail model of hand-arm vibration, a 4-hour period of vibration at 60 Hz and 49-m/s 2 acceleration generated endothelial damage, internal elastic membrane discontinuities, and smooth-muscle-cell vacuoles in the ventral artery, which were prevented by pretreatment with nifedipine, a calcium-channel blocker preventing vasoconstriction. 8,10 Vibration-induced vascular structural damage was similar to that caused by exogenous application of potent vasoconstrictors, norepinephrine and epinephrine. 17,18,29 Vibrationinduced vascular degeneration appears to be an early event.…”

Section: Hand-arm Vibration Syndrome (Havs) Involves Pe-mentioning

confidence: 86%

Effects of temperature on vibration‐induced damage in nerves and arteries

et al. 2005

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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.

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Section: Hand-arm Vibration Syndrome (Havs) Involves Pe-mentioning

confidence: 86%

Effects of temperature on vibration‐induced damage in nerves and arteries

et al. 2005

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“…Structurally similar vacuoles have been observed in SMC of arteries induced to undergo intense vasoconstriction by topical norepinephrine (NE) or epinephrine (Joris and Majno, 1977;Curry et al, 2005b;Govindaraju et al, 2006a). Joris et al, in an elegant series of electron microscopic studies, called the vacuoles herniations because the majority were continuous with the parent cell by slender necks (Joris and Majno, 1977).…”

mentioning

confidence: 85%

“…The artery was bathed in 1 mM NE in sterile Hanks' Balanced Salt Solution (Gibco) or vehicle alone for 15 min and then flushed out with Hanks solution. The concentration of NE was based on a previously published study addressing the efficacy of exogenous epinephrine and NE to induce vacuolation in the rat-tail artery (Curry et al, 2005b). The ventral artery resides in a recess bordered by tendons and skeletal muscles which prevent direct mechanical trauma during vibration.…”

Section: In Situ Tail Artery Preparationmentioning

confidence: 99%

Vibration Causes Acute Vascular Injury in a Two‐Step Process: Vasoconstriction and Vacuole Disruption

Govindaraju

Bain

Eddinger

et al. 2008

The Anatomical Record

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Hand-arm vibration syndrome is a vasospastic and neurodegenerative occupational disease. In the current study, the mechanism of vibration-induced vascular smooth muscle cell (SMC) injury was examined in a rat-tail vibration model. Tails of male Sprague Dawley rats were vibrated continuously for 4 hr at 60 Hz, 49 m/s 2 with or without general anesthesia. Ventral tail arteries were aldehyde fixed and embedded in epoxy resin to enable morphological analysis. Vibration without anesthesia caused vasoconstriction and vacuoles in the SMC. Anesthetizing rats during vibration prevented vasoconstriction and vacuole formation. Exposing tail arteries in situ to 1 mM norepinephrine (NE) for 15 min induced the greatest vasoconstriction and vacuolation. NE induced vacuoles were twice as large as those formed during vibration. When vibrated 4 hr under anesthesia after pretreatment with NE for 15 min, the SMC lacked vacuoles and exhibited a longitudinal banding pattern of dark and light staining. The extracellular matrix was filled with particulates, which were confirmed by electron microscopy to be cellular debris. The present findings demonstrate that vibration-induced vasoconstriction (SMC contraction) requires functioning central nervous system reflexes, and the physical stress of vibration damages the contracted SMC by dislodging and fragmenting SMC vacuoles. Anat Rec, 291:999

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“…Several approaches for reducing or preventing Ca 2þ influx injury have been investigated. These include increasing blood flow with Nimodipine 28 or Nifedipine 29 as well as other traditional calcium channel blockers, [30][31][32] chelators, [33][34][35] and free-radical scavangers.…”

Section: All Mammalian Cells Use Camentioning

confidence: 99%

The correlation between calcium absorption and electrophysiological recovery in crushed rat peripheral nerves

et al. 2009

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The correlation between calcium ion (Ca2+) concentration and electrophysiological recovery in crushed peripheral nerves has not been studied. Observing and quantifying the Ca2+ intensity in live normal and crushed peripheral nerves was performed using a novel microfine tearing technique and Calcium Green-1 Acetoxymethyl ester stain, a fluorescent Ca2+ indicator. Ca2+ was shown to be homogeneously distributed in the myelinated sheaths. After a crush injury, there was significant stasis in the injured zone and the portion distal to the injury. The Ca2+ has been almost completely absorbed after 24 weeks in the injured nerve to be similar to the controls. The process of the calcium absorption was correlated with the Compound Muscle Action Potential recovery process of the injured nerves. This correlation was statistically significant (r = -0.81, P < 0.05). The better understanding of this process will help us to improve nerve regeneration after peripheral nerve injury.

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Nifedipine pretreatment reduces vibration‐induced vascular damage

Cited by 16 publications

References 33 publications

Effects of temperature on vibration‐induced damage in nerves and arteries

Effects of temperature on vibration‐induced damage in nerves and arteries

Vibration Causes Acute Vascular Injury in a Two‐Step Process: Vasoconstriction and Vacuole Disruption

The correlation between calcium absorption and electrophysiological recovery in crushed rat peripheral nerves

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