Vibration and induction of endothelial injury

Blann, AD; Allen, Judith A.; McKenna, Kathleen M.; Wilder, David G.; Pope, Malcolm H.; Kaigle, Allison M.; Weinstein, L; Jayson, M. I. V.

doi:10.1016/0140-6736(92)92156-a

Cited by 9 publications

(4 citation statements)

References 5 publications

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“…Histological studies showed thickening of the muscular layer of the arteries, with hypertrophy of the muscle cells without intimal layer fibrosis. 8,9,18,35 Azuma et al 1 showed a vibration-induced hyperresponsiveness of arterial smooth muscle to nonadrenaline, and Welsh 36 demonstrated reduction of digital blood flow in the vibration frequency range of 40À200 Hz. However, the pathophysiology and mechanism of neurologic injury remain elusive.…”

Section: Discussionmentioning

confidence: 97%

Neuropathological changes in vibration injury: An experimental study

et al. 2005

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Vibration syndrome, a clinical condition arising from chronic use of vibrating tools, is associated with a spectrum of neurovascular symptoms. To date, only its vascular pathology has been extensively studied; we sought to determine what direct neurologic injury, if any, is caused by vibration. Hindlimbs of anesthetized rats were affixed to a vibrating platform 4 h a day for 7 days. Study animals were vibrated with set parameters for frequency, acceleration, velocity, and amplitude; control animals were not vibrated. On day 7, nerves were studied by light and electron microscopy. While light microscopy showed minimal histologic differences between vibrated (n=12) and control (n=12) nerves, electron microscopic changes were dramatic. Splitting of the myelin sheath and axonal damage (e.g., myelin balls and "finger ring") were consistently seen in both myelinated and nonmyelinated axons. Despite relatively short vibration, definite pathology was demonstrated, suggesting that vibration syndrome has a direct neurologic component.

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Section: Discussionmentioning

confidence: 97%

Neuropathological changes in vibration injury: An experimental study

et al. 2005

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“…HAVS results in endothelial cell damage and dysregulation 29. Humans using powered tools can exhibit elevated plasma levels of thrombomodulin, von Willebrand factor, and a reduced endothelial response to the endothelium‐dependent vasodilator, methacholine, which are consistent with endothelial damage following acute exposure to vibration 2, 19, 23, 26, 32. Long‐term maladaption to vibration causes an imbalance of constrictive and local vasoactive factors, such as nitric oxide, endothelin‐1, superoxide anion, and calcitonin gene‐related product 2, 25.…”

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confidence: 95%

Nifedipine pretreatment reduces vibration‐induced vascular damage

et al. 2005

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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.

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“…The possibility of suffering from one of the numerous syndromes that are stimulated by vibrations depends on vibration parameters and the sensitivity of the exposed individual. (Adamski 1984, Bergman 1984, Blann et al 1992, Mc Hugh et al 1993, Nagota et al 1993, Torren et al 1992. The term vibration syndrome describes all the changes in vascular and nervous as well as bone and joint systems resulting from vibrations that are usually transmitted into the hand from vibrating tools (Blann et al 1992, Blann et al 1992, Dupez et al 1992, Harrison 1993, Nowak and Nawrycz 1986.…”

Section: Introductionmentioning

confidence: 99%

“…(Adamski 1984, Bergman 1984, Blann et al 1992, Mc Hugh et al 1993, Nagota et al 1993, Torren et al 1992. The term vibration syndrome describes all the changes in vascular and nervous as well as bone and joint systems resulting from vibrations that are usually transmitted into the hand from vibrating tools (Blann et al 1992, Blann et al 1992, Dupez et al 1992, Harrison 1993, Nowak and Nawrycz 1986. Changes may occur in the limb areas or, when exposure is great, they can impact on the whole body (Harrison 1993, Hutton et al 1993, Pelmear and Taylor 1994, Pelmear and Taylor 1994.…”

Section: Introductionmentioning

confidence: 99%

Vibration syndrome diagnosis using a cooling test verified by computerized photoplethysmography

Dyszkiewicz

Tendera

2006

Physiol. Meas.

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This study addresses the problem of vibration syndrome diagnosis by means of a cooling test verified by photoplethysmography. Measurement was taken on a small area on the fingertip plexus in which many arterio-venous anastomoses are present. In the opinion of many authors, flow disorders in this area are more typical for developing vibration syndrome than changes in the micro vessels. The study group comprised 128 subjects (58 women aged 40.9 +/- 5.4 years and 70 men aged 38.7 +/- 8.8 years) exposed to vibration. The control group consisted of 41 people (20 women aged 39.6 +/- 7.3 years and 21 men aged 39.3 +/- 6.4 years) who were not exposed to vibration. The patients were examined by a questionnaire and then a vibration perception threshold test and a cooling test were performed. The cooling test was verified both visually and using the computer method. Measurement data (S1, S2 and A) for each patient were obtained from averaging three pulse graphs. We departed from an average of 60 graphs (and more), the standard established in the literature, because of the cooling test specification, which causes huge thermodynamic parameter changeability in the plexus mass of the small finger under pulse waves coming one after another. A longer measurement time will reflect the thermal drift of the tested area in a direction to compensate for the reduced temperature. In the control group, all subjects showed an increase in planimetric indicators during the cooling test verified by computerized photoplethysmography. In the study group visual verification of the cooling test was positive in eight cases (6.2%) and the vibration perception threshold test was positive in seven cases (5.5%), but in computerized photoplethysmography the planimetric indicators decreased after cooling in 87 (67.4%) cases. Computer photoplethysmography is highly specific and shows greater sensitivity in detecting preclinical forms of vascular-type vibration syndrome when compared with palesthesiometry, the visually verified cooling test and the questionnaire. The proposed test enables the detection of vascular disorders in the prodromal period and gives time for preventive measures to be taken.

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Vibration and induction of endothelial injury

Cited by 9 publications

References 5 publications

Neuropathological changes in vibration injury: An experimental study

Neuropathological changes in vibration injury: An experimental study

Nifedipine pretreatment reduces vibration‐induced vascular damage

Vibration syndrome diagnosis using a cooling test verified by computerized photoplethysmography

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