Induction of vasospastic attacks despite digital nerve block in Raynaud's disease and phenomenon.

Freedman, R. R.; Mayes, Maureen D.; Sabharwal, S. C.

doi:10.1161/01.cir.80.4.859

Cited by 37 publications

(10 citation statements)

References 14 publications

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“…This theory is consistent with RP being the result of an intrinsic problem within the blood vessels and not a result of a systemic or humoral problem. 36 For example, levels of neither epinephrine nor norepinephrine are elevated in RP sufferers, 37 , 38 and it is possible to induce an RP episode in a digit that has its sympathetic nerve output blocked; 26 , 39 facts that both allude to vascular disorder.…”

Section: Discussionmentioning

confidence: 99%

Raynaud phenomenon and mortality: 20+ years of follow-up of the Charleston Heart Study cohort

Nietert¹,

Shaftman²,

Silver³

et al. 2015

CLEP

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BackgroundRaynaud phenomenon (RP) is a temporary vasoconstrictive condition that often manifests itself in the fingers in response to cold or stress. It often co-occurs with certain chronic diseases that impact mortality. Our objective was to determine whether RP has any independent association with survival.MethodsFrom 1987–1989, a total of 830 participants of the Charleston Heart Study cohort completed an in-person RP screening questionnaire. Two definitions of RP were used: a broad definition that included both blanching (pallor) and cyanotic color changes and a narrow definition that included only blanching. All-cause and cardiovascular disease (CVD) mortality were compared between subjects with and without RP using race-specific survival models that adjusted for age, sex, baseline CVD, and 10-year risk of coronary heart disease.ResultsUsing the narrow RP definition, we identified a significant interaction between older age and the presence of RP on all-cause mortality. In the broad RP definition model, the presence of RP was not associated with CVD mortality among blacks; however, among whites, the presence of RP was associated with a 1.6-fold increase in the hazard associated with CVD-related death (hazard ratio: 1.55, 95% confidence interval: 1.10–2.20, P=0.013).ConclusionRP was independently associated with mortality among older adults in our cohort. Among whites, RP was associated with increased CVD-related death. It is possible that RP may be a sign of undiagnosed vascular disease.

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Section: Discussionmentioning

confidence: 99%

Raynaud phenomenon and mortality: 20+ years of follow-up of the Charleston Heart Study cohort

Nietert¹,

Shaftman²,

Silver³

et al. 2015

CLEP

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“…The inconsistent occurrence of the cooling‐induced contractile response suggests that specific conditions may be required for this response to occur, perhaps relating to the balance between contractile and relaxing influences existing at the time the vessel is exposed to the reduction in temperature. Even in vivo, vasospasm in response to laboratory cooling occurs only 80–90% of the time in individuals with RD (30, 31).…”

Section: Discussionmentioning

confidence: 99%

Increased tyrosine phosphorylation mediates the cooling‐induced contraction and increased vascular reactivity of Raynaud's disease

Furspan¹,

Chatterjee²,

Freedman³

2004

Arthritis & Rheumatism

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Objective. Increased levels of protein tyrosine kinase (PTK) are mechanistically associated with increased contractile responsiveness to cooling. This study tests the hypothesis that increased PTK activity mediates the increased vascular reactivity to agonists and cooling associated with primary Raynaud's disease (RD).Methods. The response of dermal arterioles isolated from control (n ‫؍‬ 29) and RD (n ‫؍‬ 29) subjects to contractile and dilatory agents at 37°C and 31°C was characterized using the microvessel perfusion technique. Fluorescence immunohistochemistry was used to measure tyrosine phosphorylation.Results. At 37°C, arteries from RD patients exhibited similar sensitivity to the specific ␣ 2 -adrenergic agonist UK 14,304, to serotonin, and to angiotensin II. At 31°C, however, the response to all 3 agonists was greater in the arterioles from the RD patients than in those from the control subjects. Agonist-induced contraction at both temperatures was reversed by cumulative addition of the PTK inhibitors genistein (1-30 M) and tyrphostin 47 (0.1-10 M). All arterioles from control subjects relaxed slightly in response to cooling, whereas more than half of those from RD patients contracted. This cooling-induced contraction was reversed by the cumulative addition of genistein. The 3 agonists elicited large increases in tyrosine phosphorylation only in arterial segments from RD patients at 31°C. Cooling from 37°C to 31°C elicited a large increase in tyrosine phosphorylation in arterioles from RD patients, but not those from control subjects. All increases in tyrosine phosphorylation could be prevented by genistein.Conclusion. Increased tyrosine phosphorylation mediates cooling-induced contraction and the increased vascular reactivity of skin arterioles from individuals with RD.

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“…This was done at the beginning and the end of the session. Wc have employed this procedure previously [16].…”

Section: Methodsmentioning

confidence: 99%

Nonneural Mediation of Digital Vasodilation during Menopausal Hot Flushes

Freedman

Woodward

Mayes

1994

Gynecol Obstet Invest

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Menopausal hot flushes are accompanied by profuse sweating, decreased skin resistance, modest tachycardia and cutaneous vasodilation. With the exception of the last effect, these events are consistent with an abrupt increase in sympathetic outflow. Blood flow in the human finger is controlled through sympathetic vasoconstricting nerves, and increased sympathetic activation results in digital vasoconstriction. We therefore sought to determine if digital vasodilation during hot flushes was mediated through efferent sympathetic nerves. Bilateral finger temperature and blood flow were recorded after the digital nerves on one hand had been blocked with a local injection of lidocaine. The effectiveness of the nerve blocks was verified by a reflex vasoconstriction test. Hot flushes were objectively defined using skin conductance responses recorded from the sternum. Fifteen hot flushes occurred in 8 women. Significant elevations in finger temperature and blood flow occurred during the flushes, in nerve-blocked and intact fingers. These findings suggest that digital vasodilation during hot flushes is due to a circulating vasodilating substance.

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Induction of vasospastic attacks despite digital nerve block in Raynaud's disease and phenomenon.

Cited by 37 publications

References 14 publications

Raynaud phenomenon and mortality: 20+ years of follow-up of the Charleston Heart Study cohort

Raynaud phenomenon and mortality: 20+ years of follow-up of the Charleston Heart Study cohort

Increased tyrosine phosphorylation mediates the cooling‐induced contraction and increased vascular reactivity of Raynaud's disease

Nonneural Mediation of Digital Vasodilation during Menopausal Hot Flushes

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