Journal
VASCULAR MEDICINE
Volume 10, Issue 4, Pages 293-307Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1191/1358863x05vm639ra
Keywords
acrocyanosis; alpha-adrenoreceptors; endothelium; estrogen; thermoregulation; vasospasm
Categories
Funding
- NHLBI NIH HHS [R01 HL63685, HL075774] Funding Source: Medline
- NIAID NIH HHS [P01 AI50153] Funding Source: Medline
- NIA NIH HHS [P01 AG18784] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL075774, R01HL063685] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI050153] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P01AG018784] Funding Source: NIH RePORTER
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Raynaud's phenomenon is due to transient cessation of blood flow to the digits of the hands or feet. An attack of Raynaud's phenomenon is classically manifested as triphasic color changes. The white phase is due to excessive vasoconstriction and cessation of regional blood flow. This phase is followed by a cyanotic phase, as the residual blood in the finger desaturates. The red phase is due to hyperemia as the attack subsides and blood flow is restored. An attack is frequently associated with pain and/or paresthesia due to sensory nerve ischemia. Variants of Raynaud's phenomenon include acrocyanosis and primary livedo reticularis, each of which is associated with reduced skin blood flow, exacerbated by cold or emotional upset. Raynaud's phenomenon in the absence of other disorders is primary Raynaud's phenomenon, or Raynaud's disease. The mechanisms of Raynaud's disease include increased activation of the sympathetic nerves, in response to cold or emotion; an impaired habituation of the cardiovascular response to stress may contribute. In addition, there appears to be a local fault, which is likely multifactorial. This local fault is due to an alteration in vascular function rather than vascular structure. The alteration in vascular function may be related to increased sensitivity to cold of the adrenergic receptors on the digital artery vascular smooth muscle. In some cases, locally released or systemically circulating vasoconstrictors may participate, including endothelin, 5-hydroxytryptamine and thromboxane. A deficiency or increased degradation of nitric oxide, possibly due to increased oxidative stress, may be involved in some cases. These recent pathophysiological insights may lead to new therapeutic options.
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