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Biomedical subjects

R R Freedman

Publications and source records attributed to R R Freedman.

At least 55 records · Page 3Linked to original sources

Physiological mechanism of digital vasoconstriction training.

Recent work in our laboratory has shown that vasodilation produced during temperature biofeedback training is mediated through a nonneural, beta-adrenergic mechanism. Here we sought to determine if the effects of feedback training for vasoconstriction are produced through a neural or nonneural pathway and whether other measures of physiological activity are correlated with these changes. Nine normal subjects received temperature feedback vasoconstriction training in which feedback was delivered only during periods of successful performance. In a subsequent session, the nerves to one finger were blocked with a local anesthetic while finger blood flow was recorded from this and other fingers. Vasoconstriction occurred during feedback in the intact fingers but not in the nerve-blocked finger and was accompanied by increased skin conductance and heart rate. These data demonstrate that temperature feedback vasoconstriction training is mediated through an efferent, sympathetic nervous pathway. In contrast, temperature feedback vasodilation training is mediated through a nonneural, beta-adrenergic mechanism.

Adult↗

Sex differences in peripheral vascular adrenergic receptors.

Although the incidence of many vascular diseases differs in men and women, sex differences in vascular physiology have not been extensively examined in human in vivo studies. The present study compared finger blood flow responses of normal men and women with brachial artery infusions of adrenergic agonists and with other neurally and nonneurally mediated procedures. In response to phenylephrine and clonidine, men showed significant dose-related vasoconstriction while women did not. In response to isoproterenol, men showed significant dose-related vasodilation while women did not. There were no sex differences in response to intra-arterial nitroglycerin or digoxin or to reactive hyperemia, procedures that do not act through adrenergic receptors. These data show that the sensitivity and/or density of peripheral vascular adrenergic receptors is lower in women than in men. There were no sex differences in response to reflex vasoconstriction or to intra-arterial tyramine, suggesting that neurally released norepinephrine acts at alpha-adrenergic receptors that are spatially removed from those that respond to circulating catecholamines.

Adult↗

EEG power spectra in sleep-onset insomnia.

EEG power spectra of 12 primary, drug-free, sleep-onset insomniacs and 12 age-matched normal sleepers were compared. Subjects slept for 3 consecutive nights in the laboratory, during which EEGs from C3A2 and O1A2 were continuously recorded on FM tape, in addition to standard EOG and EMG leads. The first unambiguous minute of record from each sleep stage, including wakefulness prior to sleep, was selected from the first sleep cycle of night 3. Analog EEG data from 0.5 to 30.5 Hz were digitized at 128 samples/sec, cosine tapered, and subjected to FFT with a resolution of 1 Hz. Sleep latencies of insomniacs (52.0 min) and normals (12.6 min) differed (P less than 0.001). There were no other sleep stage differences. Non-parametric statistics showed that, during wakefulness, insomniacs had significantly more beta activity and less alpha activity than normals. During stage 1, insomniacs had significantly more beta activity than normals. There were no differences during stages 2, 3, or 4. During REM sleep the insomniacs again had significantly more beta activity than the normals. Data from both EEG leads were generally consistent. Thus, insomniacs have increased beta and decreased alpha activity relative to normals prior to the onset of stage 2 sleep. This agrees with our previous finding of increased presleep physiological activity in insomniacs. However, the present data also suggest that a CNS component of this activity, reflected by increased beta EEG, is reactivated during REM sleep.

Adult↗

Ambulatory monitoring of panic disorder.

Twelve patients with panic disorder and 11 control subjects received 24-hour ambulatory monitoring of heart rate, finger temperature, ambient temperature, and self-rated anxiety. No differences were found between groups in tonic levels of any measure or in their patterns of variation throughout the day. However, substantial heart rate increases and finger temperature changes did occur in panic attacks but not during control periods having equally high anxiety ratings. These measures may be useful in the diagnosis of panic disorder and in the assessment of treatment outcome.

Adult↗

Effects of general and thematically relevant stressors in Raynaud's disease.

Emotional stress has been reported to cause vasospastic attacks in some patients with idiopathic Raynaud's disease. In the present study, the physiological and subjective responses of 32 Raynaud's disease patients and 22 normal subjects to three imagined scenes were compared. Both groups responded similarly to a neutral and a generally stressful scene. However, a scene having content thematically relevant to Raynaud's disease produced decreased finger temperature in these patients but not in normal controls. These findings are discussed in terms of stimulus specificity and social learning theories.

Adult↗

Behavioral treatment of Raynaud's phenomenon in scleroderma.

Twenty-four patients with Raynaud's phenomenon and scleroderma were randomly assigned to receive finger temperature biofeedback, frontalis EMG biofeedback, or autogenic training. Only those receiving temperature feedback showed significant increases in finger temperature during training and during a posttraining test of voluntary control, effects not attributable to general relaxation. However, no group demonstrated significant clinical improvement, assessed by symptom reports and by ambulatory monitoring of finger temperature. The need for careful classification of patients with Raynaud's disease and Raynaud's phenomenon in scleroderma is emphasized.

Adult↗

Psychophysiological factors in panic disorder.

Panic disorder patients were compared with normal subjects during intravenous infusion of sodium lactate, isoproterenol, and placebo. Panic attacks meeting the criteria of the Diagnostic and Statistical Manual, vol. 3 [American Psychiatric Association, 1980] occurred during all three conditions in patients and during the lactate and isoproterenol infusions in normals. Patients had significantly higher average levels of skin conductance, heart rate and state anxiety, and significantly lower finger temperatures compared to normal subjects. However, no measure reliably differentiated panic attacks from nonattack periods. It is concluded that the peripheral physiologic responses investigated are neither necessary nor sufficient for the occurrence of panic attacks. It is possible that reports of these attacks represent phobic responses to intense anxiety.

Anxiety Disorders↗

A comparison of lactate and isoproterenol anxiety states.

Both sodium lactate and isoproterenol can produce anxiety symptoms in patients with panic attacks. We administered both substances intravenously under placebo-controlled, double-blind conditions to patients with panic attacks and normal control subjects. We measured changes in anxiety levels using the Hamilton Anxiety Scale, State-Trait Anxiety Inventory, and a Panic Severity Scale. Measurements of respiratory rate and blood pH, pO2, pCO2, HCO3, and base excess were used to determine the relationship of hyperventilation to the symptoms induced by the infusions. Heart rate, epinephrine and norepinephrine levels were measured to determine whether there are changes related to palpitations and chest pain. Finger temperature and galvanic skin response were monitored to see whether any changes correlate with subject reports of hot or cold flashes and sweating. In this presentation, we will describe the clinical and biochemical changes that occur during panic attacks.

Adult↗

Role of cold and emotional stress in Raynaud's disease and scleroderma.

Research on the aetiology of Raynaud's disease and phenomenon has been hindered by the difficulty of provoking attacks in the laboratory. A study was therefore conducted in which digital and ambient temperatures, electrocardiograms, and stress ratings were obtained during ambulatory monitoring in patients with idiopathic Raynaud's disease, Raynaud's phenomenon secondary to scleroderma, and in normal subjects. In Raynaud's disease about one third of the vasospastic attacks were associated with tachycardia and increased stress ratings without declines in ambient temperature. In contrast, cold alone was enough to provoke most attacks of Raynaud's phenomenon in scleroderma. Chronically increased stress ratings in patients with scleroderma and increased muscle tension in anticipation of a cold stimulus suggest that these patients have different patterns of stress responses from those with Raynaud's disease.

Cold Temperature↗