Biomedical subjects

R R Freedman

Publications and source records attributed to R R Freedman.

63 records · Page 4Linked to original sources

PubMed1981

Biofeedback treatment of Raynaud's disease and phenomenon.

Six Raynaud's disease and four Raynaud's phenomenon patients were treated with 12 sessions of finger temperature biofeedback. The mean frequency of vasospastic attacks was reduced to 7.5% of that reported during the pretreatment baseline and was maintained for a 1 year follow-up period. Significant control of digital temperature was demonstrated during laboratory training sessions. Raynaud's phenomenon patients showed significantly greater temperature increases during feedback periods than Raynaud's disease patients. Correlations between finger temperature and other physiological measures suggested that results could not be attributed to general physical relaxation. The role of imagery in self-control of digital temperature is considered.

Adult↗

PubMed1981

A comparison of thrice weekly LAAM and daily methadone in employed heroin addicts.

Forty-eight employed heroin addicts were maintained on daily doses of methadone for four months and then randomly assigned to continue methadone maintenance or be switched to thrice weekly levo-alpha-acetylmethadol (LAAM). LAAM patients had significantly less illicit drug use and longer treatment retention times than those remaining on methadone. They also preferred LAAM to methadone on nine of 15 criteria such as the dosage schedule, feeling 'normal', and reduction of craving for heroin. LAAM may be particularly useful with employed patients owing to the reduced frequency of clinic visits.

Adult↗

PubMedDate not supplied

Physiology of hot flashes.

Hot flashes are the most common symptom of the climacteric, although prevalence estimates are lower in some rural and non-Western areas. The symptoms are characteristic of a heat-dissipation response and consist of sweating on the face, neck, and chest, as well as peripheral vasodilation. Although hot flashes clearly accompany the estrogen withdrawal at menopause, estrogen alone is not responsible since levels do not differ between symptomatic and asymptomatic women. Until recently it was thought that hot flashes were triggered by a sudden, downward resetting of the hypothalamic setpoint, since there was no evidence of increased core body temperature. Evidence obtained using a rapidly responding ingested telemetry pill indicates that the thermoneutral zone, within which sweating, peripheral vasodilation, and shivering do not occur, is virtually nonexistent in symptomatic women but normal (about 0.4 degrees C) in asymptomatic women. The results suggest that small temperature elevations preceding hot flashes acting within a reduced thermoneutral zone constitute the triggering mechanism. Central sympathetic activation is also elevated in symptomatic women which, in animal studies, reduces the thermoneutral zone. Clonidine reduces central sympathetic activation, widens the thermoneutral zone, and ameliorates hot flashes. Estrogen virtually eliminates hot flashes but its mechanism of action is not known.

Body Temperature Regulation↗

PubMedDate not supplied

Differences in alpha2-adrenoceptor modulation of calcium channels in vascular smooth muscle cells of male and female rats.

Effects of the alpha2-adrenergic agonist clonidine on current through Ca2+ channels was recorded from vascular smooth muscle cells isolated from tail arteries and aortae of male and female rats. The average Ba2+ current in control was not significantly different between males and females; however, clonidine (1 microM) enhanced Ba2+ current through Ca2+ channels in cells from females, but not from males. The greater sensitivity of vascular smooth muscle cells to clonidine may underlie different contractile responses to alpha2-adrenergic agonists between males and females.

Animals↗

PubMedDate not supplied

Nonneural beta-adrenergic vasodilating mechanism in temperature biofeedback.

Although finger temperature feedback has been used to produce digital vasodilation in normal persons and those with Raynaud's disease, the mechanism and site of this effect have not been studied. In the present investigation, feedback-induced vasodilation was attenuated by brachial artery infusions of propranolol in infused, but not contralateral, hands and was not affected by digital nerve blockade. Quantitative measurements of finger blood flow demonstrated that this vasodilation occurred in arteriovenous shunts in normal persons and in the finger capillary bed in those with Raynaud's disease. Raynaud's disease patients who received finger temperature feedback reported 80 fewer percent symptoms 1 and 2 years after treatment and retained the ability to increase finger temperature and capillary blood flow at these times. These effects were not shown by patients given autogenic training, a relaxation procedure.

Adult↗

PubMedDate not supplied

Stress-induced desensitization of alpha 2-adrenergic receptors in human platelets.

Although agonist-induced desensitization of adrenergic receptors has been previously demonstrated, the regulation of adrenergic receptors during acute psychological stress has not been investigated in humans. We studied 30 first year medical students during final examination week and one month earlier. Platelet alpha 2 receptor binding was measured using 3H-yohimbine and leukocyte beta 2 receptor binding was measured with 125I-CYP (Iodocyanopindolol). During final examination week, platelet alpha 2-receptor binding affinity was significantly reduced, while levels of plasma catecholamines and reported anxiety were significantly increased, compared with the earlier period. Students showing the greatest increases in plasma norepinephrine and in reported anxiety also demonstrated the greatest reductions in alpha 2 receptor binding affinity. These data show that acute psychological stress can produce adrenergic receptor desensitization, possibly through increased levels of circulating norepinephrine.

Adult↗

PubMedDate not supplied

Plasma catecholamines during behavioral treatments for Raynaud's disease.

We have previously demonstrated that the vasospastic attacks of Raynaud's disease can be induced despite blockade of efferent digital nerves and that feedback-induced vasodilation is mediated through a non-neural, beta-adrenergic mechanism. Here, we sought to determine the role of sympathetic activity, as measured by plasma epinephrine and norepinephrine, during finger temperature feedback and autogenic training. Thirty-one female patients with idiopathic Raynaud's disease were randomly assigned to receive finger temperature feedback or autogenic training over 28 days. Half of each group began and finished training during the follicular phase of the menstrual cycle, the other half during the luteal phase. During training, significant temperature elevations were shown by feedback patients but not by autogenic patients. There were no significant effects for norepinephrine and epinephrine for either group. Cycle phase did not interact with training effects or with catecholamines. These findings do not support the role of decreased sympathetic activation in behavioral treatments for Raynaud's disease.

Adult↗

PubMedDate not supplied

Circadian rhythm of objectively recorded hot flashes in postmenopausal breast cancer survivors.

OBJECTIVE: Similar to the circadian rhythm of core body temperature, hot flashes have been found to exhibit a circadian rhythm in healthy, naturally postmenopausal women, with a peak in frequency at 18:25 h. However, to date, no studies have evaluated whether this same pattern is found among breast cancer survivors reporting hot flashes. DESIGN: Daily hot flash frequencies were measured among 21 postmenopausal breast cancer survivors using validated 24-h sternal skin conductance monitoring. RESULTS: Hot flashes were noted in all women, ranging in frequency from 1 to 30 per 24-h period. A majority of the sample (86%) experienced > or = 1 nighttime hot flash, with 48% exhibiting > or = 3 but < or = 7 nighttime hot flashes. For the total sample, a modest circadian rhythm was noted with a peak in hot flash frequency occurring at 16:10 h. However, significant variability was observed across individual women, and, as a whole, breast cancer survivors demonstrated distorted to obliterated rhythms. CONCLUSIONS: Data suggest that hot flashes in postmenopausal breast cancer survivors do not follow the same circadian pattern as previously seen in healthy, naturally postmenopausal women. Findings have implications for (1) understanding the potential for sleep disturbances and fatigue in breast cancer survivors experiencing hot flashes, and (2) future research examining circadian rhythms of core body temperature and hot flashes in breast cancer survivors.

Body Temperature↗

PubMedDate not supplied

Hot flashes revisited.

Explore the source record for details and available documents.

Body Temperature↗