Current pathophysiological views on vibration-induced Raynaud's phenomenon

Abstract

This review attempts to summarize and discuss contemporary pathogenetic views on vibration-induced Raynaud's phenomenon assuming its multifactorial etiology. An increase in central and peripheral sympathetic nervous activity is discussed based on different physiological indicators of autonomic dysfunction and sympathetic hyperactivity. Local acral vasodysregulation is considered. Receptor and nerve endings dysfunction presented with predominance of alpha(2)-receptor function in the digital arteries and neuronal loss in those digital cutaneous perivascular nerves containing calcitonin gene-related peptide result in deficiency of endogenous release of this powerful vasodilator. Endothelial damage and dysregulation induced by vibration and increased shear stresses are demonstrated by the elevated plasma level of thrombomodulin and of von Willebrand factor and reduced endothelium-dependent vasodilator responses. The concentrations of endothelin-1 are high, the highest being in most advanced stages. Decreased plasma thiol level, indicating increased production and activity of free radicals, contribute to vasospastic paroxysms in vibration white finger patients. Dysbalance of local vasoactive factors with opposing effects on vascular smooth muscle like endothelin and nitric oxide, endothelin and calcitonin gene-related peptide, nitric oxide and superoxide anion are discussed. Disturbed smooth muscle response is supposed. Changes in hemostasis, fibrinolysis and hemorrheology, activation of blood cells with erythrocyte hyperaggregation and red cell hypodeformability, platelet aggregation with increased release of vasoconstricting thromboxane A(2) and serotonin as well as leukocyte activation, entrapment within capillaries and post-capillary venules and increased reactive oxygen species and lysosomal lytic enzymes release might also contribute to digital vasospasms and tissue damage. Elevated soluble intercellular adhesion molecule-1 levels involved in the adherence of leukocytes to endothelium and to other leukocytes have been found in patients with hand-arm vibration syndrome.

Mechanical exposure concepts using force as the agent

“…In the case of bone and articular cartilage, the process of mechanotransduction, or how cells detect strain and transduce it to a cellular response is central. Not all musculoskeletal disorders can be understood through the use of this approach; reduced blood flow with resulting localized muscle hypoxia (20) or increased tissue shear stress in hand-arm vibration resulting in damage (21,22) may need modified approaches.…”

“…Energy absorption by the tissues is used as a measure of injury potential (22) although it does seem to be related to a heating effect (21). A marker for damage would be peripheral vasospasm (an effect).…”

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

“…One of the major symptoms of HAVS is ''vibration white finger'' caused by exaggerated vasoconstriction of the arteries and skin arterioles of the hands. Many reviews implicate activation of the somatosympathetic pathway by the pacinian vibroreceptors as the reflex mechanism producing neural activation of vasoconstriction (Sakakibara and Yamada, 1995;Stoyneva et al, 2003). Finger skin biopsies from patients with HAVS reveal vascular smooth muscle cell (SMC) hypertrophy and periarterial fibrosis (Takeuchi et al, 1986).…”

Evidence for frequency-dependent arterial damage in vibrated rat tails

“…However, caution is warranted because hand-arm vibration syndrome (HAVS) continues to afflict workers using vibrating powered tools (Greenstein et al, 1991;Miyashita et al, 1995;Noel, 2000;Friden, 2001;Stoyneva et al, 2003). The disease is characterized by nervous, musculoskeletal, and vascular (white finger vasospasm) debilitating deficits in the upper extremities (Cherniack, 1990;Noel, 2000).…”