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Biomedical subjects

R R Freedman

Publications and source records attributed to R R Freedman.

At least 19 recordsLinked to original sources
PubMed1995

Blockade of vasospastic attacks by alpha 2-adrenergic but not alpha 1-adrenergic antagonists in idiopathic Raynaud's disease.

BACKGROUND: Idiopathic Raynaud's disease is characterized by cold-induced digital vasospasms, but its origin has not been established. Previous research has shown that peripheral vascular alpha 2-adrenergic receptors are hypersensitive to local cooling in these patients, but the role of alpha 1-adrenergic receptors is not clear. Moreover, the role of adrenergic receptors in the production of actual vasospastic symptoms has not been investigated. METHODS AND RESULTS: We studied 23 patients with idiopathic Raynaud's disease who were screened using conservative criteria. They were randomly assigned to receive brachial artery infusions of an alpha 1-antagonist, an alpha 2-antagonist, or both while vasospastic attacks were induced by cooling in the laboratory. Each patient's hands were photographed, and the number of attacks in the infused hand was compared with the number in the contralateral hand. The number of fingers (mean +/- SEM) with attacks in infused hands was yohimbine 0.3 +/- 0.3, prazosin 2.3 +/- 0.3, and both drugs 0.6 +/- 0.2. The difference between prazosin and the other two drug groups was significant (P < .001). CONCLUSIONS: These findings demonstrate that activation of alpha 2-adrenergic receptors but not alpha 1-adrenergic receptors is necessary for the production of vasospastic attacks in idiopathic Raynaud's disease.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1995

Core body temperature and circadian rhythm of hot flashes in menopausal women.

Postmenopausal hot flashes are characterized by sweating and peripheral vasodilation and occur more frequently during increased heat loads. The circadian rhythm of core body temperature (TC) is well known and suggests that hot flashes will be most frequent when core temperature is highest. This hypothesis has not been tested previously. Ten symptomatic and six asymptomatic postmenopausal women were recruited from advertisements and screened. Each received 24-h ambulatory monitoring of sternal skin conductance levels to detect hot flashes, ambient temperature, skin temperature, and TC. The last measure was recorded using an ingested radiotelemetry pill. Cosinor analysis demonstrated a circadian rhythm (P < 0.02) of hot flashes with a peak at about 1825 h. TC values of the symptomatic women were lower than those of the asymptomatic women (P < .05) from 0000-0400 h and at 1500 and 2200 h. The majority of hot flashes were preceded by elevations in TC. Thus, elevated TC may serve as one trigger of menopausal hot flashes.

Body Temperature↗
PubMed1994

The thermoregulatory effects of menopausal hot flashes on sleep.

Menopausal hot flashes are thought to be a disorder of thermoregulation initiated centrally within the medial preoptic area of the hypothalamus. These heat-loss mechanisms appear to be activated in the presence of normal core body temperature. Previous studies have demonstrated that thermal stimuli have the potential to alter sleep stages. We performed 24-hour ambulatory recordings of hot flashes and all-night sleep parameters on 12 postmenopausal women with hot flashes and seven postmenopausal women without flashes to determine whether the presence of hot flashes prior to sleep or during sleep itself would result in alterations in sleep pattern. The results show that hot flashes are associated with increased Stage 4 sleep and a shortened first rapid eye movement period. Hot flashes occurring in the 2 hours prior to sleep onset were positively correlated with the amount of slow-wave sleep. The central thermoregulatory mechanism underlying hot flashes may affect hypnogenic pathways inducing sleep and heat loss in the absence of a thermal load.

Body Temperature Regulation↗
PubMed1994

Nonneural mediation of digital vasodilation during menopausal hot flushes.

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.

Adult↗
PubMed1992

Behavioral treatment of menopausal hot flushes: evaluation by ambulatory monitoring.

OBJECTIVES: We attempted to develop an effective behavioral treatment for menopausal hot flushes and to determine the active behavioral components of this procedure. STUDY DESIGN: Thirty-three women with frequent menopausal hot flushes were randomly assigned to receive eight sessions of training in paced respiration, muscle relaxation, or alpha-wave electroencephalographic biofeedback (placebo control). Hot flushes were objectively measured by means of 24-hour ambulatory monitoring of the sternal skin conductance level. RESULTS: Subjects undergoing paced respiration had significant reductions in hot flush frequency and respiration rate, as well as increases in tidal volume. CONCLUSION: Paced respiration training may be a useful treatment alternative for the reduction of hot flushes in women who cannot tolerate hormone replacement therapy.

Ambulatory Care↗
PubMed1992

Local temperature modulates alpha 1- and alpha 2-adrenergic vasoconstriction in men.

Previous work in the canine saphenous vein has shown that cooling augments alpha 2- but not alpha 1-mediated contractile responses and that warming produces the opposite effects. Here we sought to determine whether these results occur in the human finger, a cutaneous vascular bed. Healthy men received brachial artery infusions of phenylephrine and clonidine with and without yohimbine while sympathetic tone was reduced by hearing the legs. Finger blood flow was recorded by venous occlusion plethysmography from two fingers, one cooled and one uncooled, on each hand. Cooling augmented alpha 2-adrenergic vasoconstriction produced by clonidine; this effect was reduced by yohimbine, an alpha 2-adrenergic antagonist. In contrast, cooling abolished alpha 1-adrenergic vasoconstriction produced by phenylephrine, which was not affected by yohimbine. Further studies were conducted in which fingers were warmed rather than cooled. Warming augmented alpha 1- but reduced alpha 2-adrenergic vasoconstriction. Thus, in human fingers, cooling augments alpha 2- and suppresses alpha 1-adrenergic vasoconstriction, whereas warming produces the opposite effects.

Adult↗
PubMed1991

Physiological mechanisms of temperature biofeedback.

Research on the physiological mechanisms of finger temperature biofeedback with normal subjects and Raynaud's disease patients is reviewed. Studies conducted in the author's laboratory have shown that feedback-induced vasodilation is mediated through a non-neural, beta-adrenergic mechanism rather than through reductions in sympathetic nervous system activation. In contrast, feedback-induced vasoconstriction is mediated through the traditional, sympathetic nervous pathway. When used with primary Raynaud's disease patients, feedback-induced vasodilation has achieved reductions in reported symptom frequency ranging from 66% to 92% in controlled investigations. Future research directions are discussed.

Biofeedback, Psychology↗
PubMed1990

Raynaud's syndrome.

Explore the source record for details and available documents.

Biofeedback, Psychology↗
PubMed1990

Alpha 2-adrenergic mechanism in menopausal hot flushes.

It has been hypothesized that hot flushes are triggered within the hypothalamus by alpha 2-adrenergic receptors on noradrenergic neurons. We administered intravenous clonidine (an alpha 2-adrenergic agonist) and yohimbine (an alpha 2-adrenergic antagonist) to nine menopausal women with hot flushes and to an asymptomatic comparison group. Hot flushes were defined objectively by skin conductance responses recorded from the sternum; finger temperature recordings and symptom reports were also evaluated. The subjects were prescreened using ambulatory skin conductance monitoring. A significantly greater number of hot flushes occurred during yohimbine sessions than in corresponding placebo sessions (six versus zero). Clonidine significantly increased the amount of peripheral heating needed to provoke a hot flush (40.6 versus 33.6 minutes) and reduced the number of hot flushes that did occur (two versus eight). No hot flushes occurred in the asymptomatic women. These findings support the role of a central alpha 2-adrenergic mechanism in the initiation of hot flushes.

Adult↗
PubMed1989

Increased alpha-adrenergic responsiveness in idiopathic Raynaud's disease.

In our study of 28 patients with idiopathic Raynaud's disease, the patients had significantly greater digital blood flow responses to intraarterial phenylephrine and clonidine than did normal control subjects. There were no group differences in finger blood flow responses to body heating, reflex cooling, digital ischemia, or to intraarterial tyramine or isoproterenol. There were also no group differences in blood pressure or heart rate during any procedure. These results suggest that patients with idiopathic Raynaud's disease have increased peripheral vascular alpha-adrenergic receptor sensitivity and/or density compared with normal persons.

Adult↗
PubMed1989

Laboratory and ambulatory monitoring of menopausal hot flashes.

A large increase in skin conductance activity recorded from the sternum was found during menopausal hot flashes and corresponded well with patient self-reports. The magnitude and time course of this skin conductance change was similar during spontaneous hot flashes recorded in the laboratory, during heat-induced hot flashes, and during those recorded by ambulatory monitoring techniques. This pattern of sternal skin conductance change did not occur in premenopausal women during body heating or ambulatory monitoring. These methods should be useful in research on the etiology and treatment of menopausal hot flashes.

Adult↗
PubMed1989

Quantitative measurements of finger blood flow during behavioral treatments for Raynaud's disease.

Quantitative measurements of finger blood flow have not been performed during temperature biofeedback or other treatments for Raynaud's disease. In the present investigation, finger blood flow was determined with venous occlusion plethysmography, in addition to measurements of finger temperature, heart rate, blood pressure, and skin conductance level. After a maximum vasodilation test, subjects received 10 sessions of finger temperature biofeedback or autogenic training. There were no group differences during the maximum vasodilation test. During training, temperature feedback subjects showed significant elevations in finger blood flow, finger temperature, and skin conductance level, whereas those who received autogenic training did not. These findings could not be explained by group differences in other cardiovascular measures and are consistent with previous studies suggesting the involvement of an active vasodilating mechanism in temperature feedback.

Adult↗
PubMed1989

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

Using a combination of environmental and local cooling, we induced vasospastic attacks of Raynaud's phenomenon in nine of 11 patients with idiopathic Raynaud's disease and in eight of 10 patients with scleroderma. Attacks were defined as occurring if two of the possible three color changes (pallor, cyanosis, and rubor) occurred, and serial photographs were scored by three independent raters. Two fingers on one hand were anesthetized by local injection of lidocaine, and the effectiveness of nerve blocks was verified by plethysmography. The frequency of vasospastic attacks in nerve-blocked fingers was not significantly different from that in the corresponding intact fingers on the contralateral hand. These findings show that the vasospastic attacks of Raynaud's disease and phenomenon can occur without the involvement of efferent digital nerves and argue against the etiologic role of sympathetic hyperactivity.

Cold Temperature↗