Search PubMed⌕ Search

Biomedical subjects

D B Carr

Publications and source records attributed to D B Carr.

At least 127 records · Page 7Linked to original sources
PubMed1985

Effects of neuroleptic drugs on brain beta-endorphin immunoreactivity.

The effect of chronic haloperidol on brain beta-endorphin immunoreactivity was examined in rats. Chronic haloperidol resulted in significant reductions of beta-endorphin immunoreactivity within the striatum, but other brain regions were uneffected. When a variety of neuroleptic drugs were tested, fluphenazine, chlorpromazine and haloperidol resulted in comparable reductions in beta-endorphin immunoreactivity in the striatum. These findings suggest a functional interaction between beta-endorphin and dopamine systems in the striatum.

Animals↗
PubMed1985

Causal links between plasma and CSF endorphin levels in stress: vector-ARMA analysis.

To explore causal links between vital sign responses and immunoreactive beta-endorphin ("i-BE") rises in blood and CSF during ovine endotoxin stress, we analyzed concurrent i-BE levels in these two compartments by a "vector-ARMA" (= autoregressive moving average) method. This technique--widely used for modeling in other applications--has not to our knowledge been employed to study dynamic relationships of neuropeptides. Log-transformed i-BE levels were first "filtered" by repeated observations ANOVA to confirm significance of rises in both compartments. Next, vector-ARMA methodology was applied to derive an optimal causal model of vital sign changes and i-BE entry into plasma vs. CSF pools. The model indicated that reflux of i-BE from blood into CSF contributed to increases in CSF levels of this hormone. This novel application to neuroendocrinology of this approach illustrates its utility in evaluating changes in one or more neuropeptide levels in multiple compartments to indicate potentially causal relationships.

Animals↗
PubMed1985

Endogenous opioids and ventilatory responses to hypercapnia in normal humans.

Though administration of opioid peptides depresses ventilation and ventilatory responsiveness, the role of endogenous opioid peptides in modulating ventilatory responsiveness is not clear. We studied the interaction of endogenous opioids and ventilatory responses in 12 adult male volunteers by relating hypercapnic responsiveness to plasma levels of immunoactive beta-endorphin and by administering the opiate antagonist naloxone. Ventilatory responsiveness to hypercapnia was not altered by pretreatment with naloxone, and this by itself suggests that endogenous opioids have no role in modulating this response. However, there was an inverse relationship between basal levels of immunoactive beta-endorphin in plasma and ventilatory responsiveness to CO2. Furthermore, plasma beta-endorphin levels rose after short-term hypercapnia but only when subjects had been pretreated with naloxone. We conclude that measurement of plasma endorphin levels suggests relationships between endogenous opioid peptides and ventilatory responses to CO2 that are not apparent in studies limited to assessing the effect of naloxone.

Adult↗
PubMed1985

Endogenous opioids and ventilatory responses to hypoxia in normal humans.

We studied the putative role of endorphins in modulating hypoxic ventilatory responsiveness. In 12 healthy men, minute ventilation (VE)and mouth occlusion pressure (P0.1) responses to progressive isocapnic hypoxia were determined before and after the intravenous administration of the opioid antagonist naloxone (10 mg) or placebo. Plasma levels of beta-endorphin were measured before and after hypoxia. Naloxone did not affect the slopes or x-intercepts of the relationships between either VE or P0.1 and arterial O2 saturation. There was no correlation between the baseline plasma level of beta-endorphin and any measure of responsiveness to hypoxia. Plasma beta-endorphin levels were not affected by either short-term hypoxia or naloxone alone; however, when hypoxia followed naloxone administration, mean +/- SD beta-endorphin increased from 8.0 +/- 8.9 pg/ml to 20.2 +/- 16.6 pg/ml (p less than 0.005). We concluded that endogenous opioids do not have an important modulating influence on hypoxic ventilatory responsiveness in adult human volunteers.

Adult↗
PubMed1985

Contrasting actions of naloxone in experimental spinal cord trauma and cerebral ischemia: a review.

Endorphins have been implicated in the pathophysiology of both spinal cord injury and cerebral ischemia. This review examines the nature of the experimental evidence to support this hypothesis. Present studies suggest that naloxone administration improves neurological function and outcome in the setting of the spinal cord trauma by centrally inhibiting an opiate receptor-mediated diminution of spinal cord flow. In the setting of spinal shock, naloxone administration is associated with improvement in vital sign and cardiovascular parameters as measured by mean arterial pressure, cardiac output, body temperature, and ventilation. Experiments using a variety of animal stroke models similarly support the notion that naloxone improves neurological function in the setting of cerebral ischemia by a stereospecific opiate receptor-mediated effect, but this improvement does not seem to be accompanied by augmentation of blood flow to affected areas of the brain or by any improvement in vital signs or cardiovascular parameters as seen in spinal cord trauma. A variety of mechanisms are discussed to explain these observations. The therapeutic implications of administering opiate agonists and antagonists in the setting of neurological deficits are outlined for the neurosurgeon.

Animals↗
PubMed1985

Lactate infusion in anxiety research: its evolution and practice.

The unpredictability of spontaneous unexpected panic attacks has inhibited the controlled study of this phenomenon. Previous studies demonstrated that an increase in blood lactic acid occurred concomitant with symptoms of anxiety in anxiety-prone patients who underwent standard physical exercise. The question of whether these patients had an excessive sensitivity to lactate led to the development of the lactate infusion model, in which anxiety is induced in a controlled environment. The history and current application of the lactate infusion model in the study of neurochemical correlates of panic are described, and a methodology for lactate infusion procedures is outlined.

Anxiety Disorders↗
PubMed1985

Thyroid indices in panic disorder.

Eighty-two patients suffering from panic attacks with or without phobias were examined for evidence of thyroid disease. None of the patients had abnormal total T4 or T3 resin uptake measurements, regardless of whether they were nonmedicated or treated with one of three antipanic drugs: alprazolam, phenelzine, or imipramine. A higher than expected incidence of undetectable TSH levels (22% overall) appeared in all groups. The clinical relevance of this finding is currently uncertain.

Adult↗
PubMed1984

Neuroendocrine effects of caffeine in normal subjects.

In double-blind crossover experiments, we examined the effects of oral caffeine (250 or 500 mg) added to decaffeinated coffee on plasma hormone levels in adults who normally consume one to three cups of coffee a day. In one experiment, 250 mg (about 4 mg/kg) caffeine was given to men; in two other experiments, 500 mg (8 mg/kg) was given to both sexes. Caffeine, 500 mg, elevated plasma levels of beta-endorphin-like immunoreactivity in both men and women but had no significant effect on plasma levels of cortisol, thyroid-stimulating hormone, growth hormone, prolactin, or triiodothyronine in men nor on plasma levels of prolactin or cortisol in women. The 250-mg dose induced no significant changes in plasma levels of any of the hormones measured. We conclude that the threshold for caffeine's endocrine effects is higher than that for its behavioral effects.

Administration, Oral↗
PubMed1984

Endurance training effects on plasma hormonal responsiveness and sex hormone excretion.

A prospective study of the hormonal effects of a moderate exercise training program (4-wk control, 8-wk training) was conducted in seven young women. Sixty-minutes continuous bicycle ergometer tests of fixed relative intensity were performed at the beginning, middle, and end of the training period. The capacity of these acute bouts of exercise to affect circulating levels of stress markers, reproductive hormones, and hormones with possible antireproductive potential was measured. In addition, the urinary excretion of reproductive hormones was monitored continuously via serial overnight urine collections. Within testing sessions, plasma concentrations of all stress markers and antireproductive hormones rose significantly. Across testing sessions, only beta-endorphin + beta-lipotropin and cortisol exhibited an increment in peak responses as training progressed. Plasma reproductive hormone levels showed insignificant acute changes, and cyclic menstruation and preovulatory gonadotropin surges continued in all subjects. However, ovarian function was disturbed in four subjects as evidenced by a decreased excretion of estriol, free progesterone, or both. Transient infertility is a known clinical accompaniment of hormonal changes of comparable subtlety.

Adolescent↗
PubMed1984

Rate-sensitive inhibition of ACTH release in depression.

Rate-sensitive inhibition of ACTH release is abnormal in Cushing's disease but uncharacterized in depression. The authors found that two of 10 depressed patients had paradoxical responses, suggesting the existence of a hypothalamic-pituitary-adrenal axis abnormality in depression that is independent of dexamethasone suppression test results.

Adrenocorticotropic Hormone↗
PubMed1984

Panic anxiety: a new biological model.

Previously unrecognized similarities among metabolic responses to various maneuvers used to evoke anxiety in patients with panic disorder are described. On the basis of these observations, a new biological model is proposed for panic disorder, in which the primary defect--which is neuroendocrine rather than psychiatric--is operationally placed within the redox-regulating apparatus of the brain stem. This model is consistent with many clinical features of panic disorder and also provides a theoretical framework for further studies of the pathophysiology of this and related conditions (e.g., hyperventilation syndrome).

Anxiety Disorders↗
PubMed1984

Identification of speech disorders.

This article focuses on the early identification and referral of children who may have speech disorders. A distinction is made between speech and language, i.e., speech is the spoken vehicle by which we communicate our thoughts, as expressed symbolically through language. The evaluation of speech should be performed systematically by the assessment of four basic components of speech: phonation, resonance, articulation, and prosody. Suggestions regarding management and referral are presented.

Articulation Disorders↗
PubMed1983

Naloxone blocks exercise-stimulated water intake in the rat.

To examine whether opiate receptors modulate exercise-induced water intake, we measured water intake during four consecutive hours after a one-hour swim stress in male, Sprague-Dawley rats. Increased cumulative water intake was found four hours following exercise and this response was naloxone-reversible (P = 0.06). Suppression of water intake in the naloxone-treated, exercised group was most marked in the first two hours after exercise (P less than 0.05). Non-exercised rats consumed water at a constant, linear rate (P less than 0.05) whether treated with naloxone or saline. These results indicate an endogenous opioid role in regulating exercise-induced water intake in the rat, but do not delineate whether this role reflects a non-specific stress behavior or specific physiological processes related to thirst.

Animals↗
PubMed1983

Perinatal exposure to 60-Hz electric fields: effects on the development of the visual-evoked response in rats.

Two independent series of experiments were performed on 114 male Sprague-Dawley-derived, albino rat pups, which represented 61 litters in experimental series I and 53 litters in experimental series II. Animals were exposed for 20 h/day from conception to testing (postnatal days 11-20) to a vertical, 65-kV/m, 60-Hz electric field or sham-exposed. Recordings of the visual-evoked response (VER) were obtained using a small silver ball electrode placed epidurally over the visual cortex. Visual stimuli consisted of 10-microseconds light flashes delivered at 0.2 Hz. Computer-averaged VERs were obtained and power spectral analyses (fast Fourier transform) were performed on the tapered (split cosine-bell window), averaged VERs. The expected age-related changes were clearly evident; however, a detailed analysis of VER component latencies, peak-to-peak amplitude, and power spectra failed to reveal any consistent, statistically significant effect of exposure to 60-Hz electric fields.

Animals↗
PubMed1983

Changes in cerebrospinal fluid and plasma vasopressin in the febrile sheep.

Plasma and cerebrospinal fluid (CSF) concentrations of vasopressin (AVP) were measured in conscious sheep during fever induced by iv endotoxin. Body temperature and blood pressure were also measured. AVP concentrations increased in both CSF and plasma although increases were not parallel. AVP concentrations in CSF were significantly correlated to increases in body temperature whereas plasma AVP concentrations were not. Neither CSF nor plasma AVP concentrations were correlated with changes in blood pressure. These data indicate that there may be independent regulation of AVP release into plasma and CSF compartments and supports the idea that AVP may have several physiological functions to perform during fever.

Animals↗
PubMed1983

The effects of cysteamine on thyrotropin and immunoreactive beta-endorphin secretion in the rat.

We examined the effects of the thiol agent cysteamine (CSH), which is known to deplete the hypothalamus of immunoreactive somatostatin, on physiological TSH and beta- endorphin secretion in the adult male rat. CSH at doses of 90 and 300 mg/kg CSH produced a rapid decline in plasma TSH, whereas a dose of 30 mg/kg did not alter plasma TSH levels. After the higher doses of CSH, TSH levels in the blood remained lower than control values on day 2, but returned to normal by 1 week. This decrease in TSH within the plasma was not associated with a reduction in hypothalamic TRH concentrations. The TSH response to 500 ng/kg TRH was normal in CSH-treated animals. Blockade of norepinephrine synthesis with diethyldithiocarbamate (500 mg/kg) or fusaric acid (100 mg/kg) inhibited TSH secretion in a manner similar to that of CSH. beta-Endorphin-like immunoreactivity (bet-End-LI) was elevated in the plasma immediately after CSH (300 mg/kg) administration. This was associated with a 58% reduction in anterior pituitary beta-End-LI and no change in hypothalmic beta-End-LI. Plasma beta-End-LI returned to normal on day 2. The increase in plasma beta-End-LI induced by immobilization stress was not compromised by CSH treatment. The observed effects of CSH on both TSH and beta-End-LI are consistent with a reduction in central norepinephrine neurotransmission through the known actin of CSH to inhibit dopamine-beta-hydroxylase. Acute stress may play a role as well in the observed changes in TSH and beta-End-LI secretion.

Animals↗
PubMed1983

Dynamics of cortisol and endorphin responses to graded doses of synthetic ovine CRF in sheep.

Corticotropin-releasing factor (CRF), recently isolated from sheep hypothalami, has been shown to stimulate secretion of ACTH and beta-endorphin in vitro, and in vivo in rat and man. In previous reports, responses to ovine CRF were studied in heterologous bioassay systems where the ovine sequence was likely to act as a CRF analogue. We administered synthetic ovine CRF to sheep to assess the dynamics of endorphin and cortisol responses. Graded doses of CRF caused a rapid increase in immunoreactive beta-endorphin (iB-E) within 2 min of iv administration, followed by a cortisol response which was maximal 15 min after the iB-E peak. Doses of CRF in excess of 10 micrograms did not increase the magnitude of the peak iB-E response but did prolong the duration of the plasma beta-endorphin rise. Ovine CRF is an extremely potent and rapidly-acting hypothalamic peptide in vivo when assayed in a homologous system.

Animals↗