Plasma free and intraplatelet serotonin in patients with Raynaud's phenomenon

Biondi, Maria Luisa; Marasini, Bianca; Bianchi, E.; Agostoni, A

doi:10.1016/0167-5273(88)90238-0

Cited by 59 publications

(35 citation statements)

References 12 publications

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“…54 Furthermore, in one study, levels of 5-HT in plasma and in platelets were elevated in primary Raynaud's patients. 55 However, a later study showed that plasma levels of 5-HT were no higher in primary Raynaud's patients than controls and cooling did not change the arteriovenous difference for 5-HT across the forearm in either primary Raynaud's patients or controls. Further, in three primary Raynaud's patients, there was no release of 5-HT into the venous efflux during a period of vasospasm.…”

Section: -Hydroxytryptamine (5-ht Serotonin)mentioning

confidence: 99%

Mechanisms of Raynaud’s disease

2005

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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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Section: -Hydroxytryptamine (5-ht Serotonin)mentioning

confidence: 99%

Mechanisms of Raynaud’s disease

2005

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“…67 Serotonin, another circulating vasoconstrictor released from platelets, has also been reported to be significantly elevated in patients with Raynaud's phenomenon. 68 However, these factors might be a consequence rather than a cause of vascular damage. Thromboxane A 2 increases in proportion to the severity of disease in secondary Raynaud's disease.…”

Section: Platelet Activationmentioning

confidence: 99%

Raynaud's phenomenon: Pathogenesis and management

Bakst

Merola

Franks

et al. 2008

Journal of the American Academy of Dermatology

161

139

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“…Although the pathogeneses of peripheral circulation disorders have not been completely determined, hypercoagulability may be involved [4]. Hypercoagulability of the blood is thought to be caused by a variety of mechanisms, such as enhancement of platelet agglutination activity [18], decreased deformability of erythrocytes [19], and vascular endothelial cell injury [20]. It has been found that platelets are hyperactivated under these pathological conditions [21].…”

Section: Discussionmentioning

confidence: 99%

Effect of Ticlopidine on Platelet-Derived Microparticles in Patients with Connective Tissue Diseases

Kagawa

Nomura²,

Nagahama³

et al. 1999

Pathophysiol Haemos Thromb

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We evaluated the plasma concentrations of platelet activation markers and platelet-derived microparticles (PMP) in patients with connective tissue diseases complaining of peripheral circulation disorders (n = 16) and studied the effect of ticlopidine hydrochloride (ticlopidine) on PMP generation. There were significant differences in the levels of PMP and a platelet activation marker between before and after treatment with ticlopidine (PMP: 695 ± 393 vs. 354 ± 206/10⁴ platelets, p < 0.01; platelet CD63: 9.13 ± 5.64 vs. 5.22 ± 2.74%, p < 0.05). On the other hand, markers of vascular endothelium, such as vascular endothelium-derived small vesicles and serum thrombomodulin levels, were not affected by the administration of ticlopidine. Levels of cytokines and soluble adhesion molecules remained unchanged by ticlopidine administration. These findings suggest that ticlopidine may be useful for the inhibition of PMP-dependent vascular damage in patients with connective tissue diseases complaining of peripheral circulation disorders.

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Plasma free and intraplatelet serotonin in patients with Raynaud's phenomenon

Cited by 59 publications

References 12 publications

Mechanisms of Raynaud’s disease

Mechanisms of Raynaud’s disease

Raynaud's phenomenon: Pathogenesis and management

Effect of Ticlopidine on Platelet-Derived Microparticles in Patients with Connective Tissue Diseases

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