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Biomedical subjects

J L Abelson

Publications and source records attributed to J L Abelson.

32 records · Page 2Linked to original sources
PubMed1992

Endocrine, cardiovascular, and behavioral responses to clonidine in patients with panic disorder.

We examined adrenergic regulation in patients with panic disorder by challenging 10 patients and 14 age-matched and sex-matched controls with intravenous infusions of clonidine hydrochloride (2 micrograms/kg), an alpha 2-adrenoreceptor agonist. Growth hormone, 3-methoxy-4-hydroxyphenylglycol (MHPG), blood pressure, heart rate, and behavioral (anxiety, sedation) responses were monitored. The data replicated the previously reported finding of blunted growth hormone (GH) responses to clonidine in patients with panic disorder. Reported abnormalities in MHPG, cardiovascular, and behavioral responses of panic patients to clonidine infusion were not replicated. The robustly blunted GH response to clonidine in panic patients supports the adrenergic dysregulation hypothesis of panic disorder, but alternative interpretations of this finding are available and further study is needed.

Adrenergic Fibers↗
PubMed1991

Blunted growth hormone response to clonidine in patients with generalized anxiety disorder.

Patients with panic disorder or depression have abnormal responses to the alpha 2-adrenergic receptor partial agonist clonidine. Evidence linking anxiety to noradrenergic dysfunction and the presence of anxiety symptoms in both depression and panic suggest that abnormal responses to clonidine in these disorders could be due to the anxiety symptoms. To explore a possible link between "nonspecific" anxiety symptoms and abnormal responses to clonidine, patients with DSM-III-defined generalized anxiety disorder were given intravenous infusions of clonidine hydrochloride. Responses of plasma growth hormone, 3-methoxy-4-hydroxyphenylglycol, heart rate, blood pressure, and psychological states were determined in 11 patients with generalized anxiety disorder and 14 healthy subjects. Clonidine produced significantly smaller growth hormone responses in patients than in healthy controls. The two groups did not differ in 3-methoxy-4-hydroxyphenylglycol, heart rate, blood pressure, or psychological responses to clonidine. These results are compared with data from similar studies on patients with panic disorder and depression. The blunting of the growth hormone response to clonidine in all three disorders could be due to the presence of generalized anxiety symptoms. Subsensitivity of postsynaptic alpha 2-adrenoreceptors may be present in all three disorders; however, there are alternative interpretations of growth hormone blunting in response to clonidine. Blunting was observed in DSM-III-defined generalized anxiety disorder, whether or not the DSM-III-R criterion of excessive worry was also present.

Adult↗
PubMed1990

Alpha 2-adrenoreceptor status in obsessive-compulsive disorder.

Ten patients with obsessive-compulsive disorder (OCD) and 13 normal control subjects received intravenous infusions of 2 X 10(-6) g/kg of clonidine and normal saline on separate days. Responses to the drug relating to plasma growth hormone (GH), 3-methoxy-4-hydroxyphenylglycol (MHPG), heart rate, blood pressure, and several symptoms were determined. Additionally, platelet alpha 2-adrenoreceptor binding was measured in most of the subjects. GH, MHPG, blood pressure, and heart rate responses to clonidine did not differ between groups. As expected, patients reported more symptoms than normal subjects, and clonidine was sedating for both groups. Patients did not differ from normal subjects in the symptom response to clonidine. The maximum number of binding sites (Bmax) for tritiated clonidine was significantly greater in OCD patients than in normals. This pattern of alpha 2-adrenoreceptor status is different than the patterns in major depression and panic anxiety.

Adult↗
PubMed1990

Treatment of panic-like attacks with a long-acting analogue of somatostatin.

Psychiatric evaluations were completed on four patients who were treated for "idiopathic flushing" with a long-acting analogue of somatostatin. All four patients had symptom profiles consistent with a diagnosis of panic disorder. All four experienced clinically significant relief from panic-like attacks while on the experimental medication. These findings suggest a possible role for somatostatin in the pathophysiology and treatment of panic disorder.

Adult↗
PubMed1989

Cardiac and neuroendocrine responses to exposure therapy in height phobics: desynchrony within the 'physiological response system'.

Subjective, behavioral, cardiovascular and neuroendocrine responses were intensively monitored in two height phobics over a full course of exposure therapy and at follow-up. Both subjects showed rising cortisol responses and stable, non-extinguishing norepinephrine responses to height exposure over the course of treatment, while improvement occurred in subjective and behavioral response systems. They had differing heart rate responses. Despite desynchrony amongst anxiety response systems and within the physiological 'system' at treatment conclusion, both subjects had successful outcomes which were preserved at follow-up. Implications for the measurement of the 'physiological response system' in behavioral research are discussed.

Adult↗
PubMed1983

Interpersonal and electrocardiographic responses of Type A's and Type B's in competitive socioeconomic games.

Forty-eight subjects classified as either Type A (coronary-prone) or Type B (coronary-resistant) exchanged points worth money with a computer-simulated opponent while an electrocardiogram was computer-monitored and scored. Type A's were more aggressive during the socioeconomic exchanges than were Type B's. The more aggressive a subject during the interactions the greater was the shift toward depression of the ST segment of the electrocardiogram. Despite the relationship between aggression and ST response, and the greater aggressiveness of Type A's during the interactions, Type A's and Type B's did not differ significantly in ST response.

Adult↗
PubMedDate not supplied

Cholecystokinin in psychiatric research: a time for cautious excitement.

Cholecystokinin (CCK) is a peptide neurotransmitter that was originally isolated from the gastrointestinal system, but which is extensively and abundantly distributed within the central nervous system (CNS). Stimulated by the fairly recent recognition of receptor subtypes (A and B), and the development of receptor-specific antagonists, CCK research has been advancing rapidly; and its potential importance to psychiatric neuroscience has been increasingly recognized. CCK participates in the mediation of satiety; it interacts with dopamine and may modulate psychosis; it interacts with opiate systems and may be an "anti-analgesic": and it appears to play a role in the mediation of anxiety. Highly specific, CCK-B receptor antagonists have reached clinical trials and have potential clinical utility as anxiolytics, antipsychotics, anti-anorexics, or analgesics. There are grounds for excitement, but many obstacles remain to be overcome and clinical potential may not be fulfilled. However, we must not allow clinical disappointments to slow the accelerating pace of scientific progress in CCK research. Regardless of clinical payoffs, the CCK receptor is clearly of great importance to human CNS functioning and deserves ongoing scientific attention.

Anxiety Disorders↗
PubMedDate not supplied

Hypothalamic-pituitary-adrenal axis activity in panic disorder: effects of alprazolam on 24 h secretion of adrenocorticotropin and cortisol.

Pre-clinical and some clinical evidence suggests that central overdrive within the hypothalamic-pituitary-adrenal (HPA) axis may play a role in panic disorder, and that the anti-panic efficacy of alprazolam may involve its ability to inhibit this drive. Detailed examination of 24 h secretion of adrenocorticotropin (ACTH) and cortisol in 20 panic patients had revealed subtle HPA axis abnormalities prior to treatment. In order to determine whether these abnormalities resolve with alprazolam therapy, these patients were re-studied over a full circadian cycle after 12 weeks on alprazolam. Alprazolam produced substantial improvement in clinical status which was accompanied by nearly full resolution of pre-treatment hypercortisolemia. The impact of treatment on ACTH was more complex and influenced by symptom severity. The results are consistent with the hypotheses that HPA axis regulation is subtly disturbed in panic disorder and that impact on the HPA axis may play a role in alprazolam's mechanism of efficacy.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Respiratory psychophysiology and anxiety: cognitive intervention in the doxapram model of panic.

UNLABELLED: The goals of this study were to: a) confirm prior evidence that the respiratory stimulant doxapram induces panic attacks and produces excessive hyperventilation in patients with panic disorder and b) explore the impact of cognitive mediators on symptom and respiratory responses. METHOD: Thirty-two subjects (16 patients and 16 controls) received doxapram (0.5 mg/kg) and placebo infusions while symptom, respiratory, and heart rate responses were monitored. Subjects were randomly assigned to receive either a standard introduction or a cognitive intervention designed to reduce the panic responses of panic patients to laboratory challenges. RESULTS: Doxapram was a potent and specific panicogenic agent, inducing panic in 75% of patients and 12.5% of controls. Compared with controls, patients also showed a greater decrease in end tidal carbon dioxide (CO2) and greater increases in minute ventilation, respiratory frequency, and heart rate. The cognitive intervention substantially attenuated the excessive hyperventilatory response of patients but did not fully normalize their breathing patterns. Tidal volume was the only respiratory measure not significantly altered by the cognitive intervention. CONCLUSIONS: In patients with panic disorder, doxapram (0.5 mg/kg) triggers panic attacks about as potently as 7% CO2 and more potently than 5% CO2 or lactate. Psychological factors can modulate the appearance of ventilatory abnormalities in panic patients, but persistent respiratory disturbances were still seen. Psychological factors and respiratory physiology both appear to be important phenomena in laboratory panic.

Adult↗