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Biomedical subjects

S C Risch

Publications and source records attributed to S C Risch.

At least 91 records · Page 5Linked to original sources
PubMed1986

Neuroendocrine responses in psychiatric and pain patients with major depression.

Basal and postdexamethasone concentrations of cortisol and prolactin were studied in three groups of male patients: chronic pain patients with no psychiatric diagnosis (n = 12), chronic pain patients with coexisting major depression by Research Diagnostic Criteria (RDC) (n = 24), and pain-free psychiatric patients meeting RDC criteria for major depression (n = 28). Basal cortisol concentrations were significantly higher in pain-major depression and psychiatric-major depression patients compared to pain patients without psychiatric illness. The frequency of cortisol nonsuppression after dexamethasone was significantly greater in pain patients with major depression (41.7%) compared to pain patients without psychiatric disorder (8.3%), and was comparable to that of psychiatric patients (21.4%). Prolactin concentrations, but not cortisol levels, were significantly correlated with observer-rated severity of depression in pain patients. These findings suggest that cortisol and prolactin abnormalities in chronic pain may be related to psychiatric disorder rather than to pain per se, at least in male patients, and may indicate a role for cholinergic mechanisms in the interface of pain and depression.

Adult↗
PubMed1986

A kinetic analysis and replication of decreased platelet serotonin uptake in depressed patients.

Platelet serotonin uptake was kinetically measured in 32 psychiatric inpatients and 32 age- and sex-matched controls. Patients were categorized into four groups: depressed patients, manic bipolars, other affective disorders, and nonaffective psychiatric disorders. A randomized block factorial analysis of variance indicated that the depressed patients had a significantly lower maximal velocity (Vmax) of serotonin uptake in comparison to matched controls, without a statistically significant difference in Km. No statistically significant difference was found for any of the other diagnostic groups in comparison to controls for Vmax or Km. These results are compared with previous studies of platelet serotonin transport in clinically depressed patients and in physostigmine-induced depression.

Bipolar Disorder↗
PubMed1986

Central and peripheral cholinesterase inhibition: effects on anterior pituitary and sympathomimetic function.

Ten physically healthy inpatients of mixed diagnosis received, in a randomized, counterbalanced double-blind paradigm, physostigmine (22 micrograms/kg) and neostigmine (11 micrograms/kg). Infusions were separated by at least 2 days. The differential effects of physostigmine and neostigmine on plasma concentrations of cortisol, prolactin, growth hormone, ACTH, beta-endorphin/beta-lipotropin-like immunoreactivity, dopamine, norepinephrine, and epinephrine are reported. Administration of physostigmine, unlike that of neostigmine, was associated with statistically significant increases in plasma concentrations of cortisol, prolactin, ACTH, beta-endorphin/beta-lipotropin-like immunoreactivity, and epinephrine, presumably via central mechanisms. In a separate study, 15 subjects, mostly depressed inpatients, were pretreated with methscopolamine (0.75 mg) on one day and scopolamine (0.5 mg) on another day, at least 2 days apart, in a randomized, counterbalanced double blind paradigm and subsequently on each day received physostigmine (22 micrograms/kg). Scopolamine significantly attenuated the physostigmine-associated increase in plasma concentrations of cortisol, growth hormone, prolactin, ACTH, and dopamine compared to methscopolamine, and a close-to-significant attenuation of epinephrine as well. These results provide further evidence that physostigmine's effects on plasma concentrations of pituitary hormones and epinephrine occur via central mechanisms and are muscarinically mediated.

Adrenocorticotropic Hormone↗
PubMed1986

Physostigmine-induced epinephrine release in patients with affective disorder.

Infusion of the cholinomimetic drug physostigmine led to profound increases in serum epinephrine levels and slight increases in serum norepinephrine levels among 38 patients with affective disorder and 22 control subjects. Preliminary results suggest that physostigmine may induce relatively blunted increases in serum epinephrine levels in patients with affective disorders.

Adult↗
PubMed1985

Physostigmine effects on serotonin uptake in human blood platelets.

Platelet serotonin (5HT) uptake was measured in 18 subjects administered physostigmine salicylate in a double-blind, placebo crossover design. In comparison to placebo, the drug caused a significant transient depression in mood, as measured by self- and observer-rated depression scores. In addition, physostigmine significantly increased platelet counts while independently decreasing the maximum velocity (Vmax) of platelet serotonin uptake. Physostigmine administration did not significantly affect the affinity constant (Km) for platelet serotonin uptake. The data are interpreted as being consistent with the postulate that platelet serotonin uptake may be decreased in depressed patients via cholinergic mechanisms.

Blood Platelets↗
PubMed1985

Antagonism of physostigmine induced lethality by a combination of scopolamine and methscopolamine.

The antagonistic effects of scopolamine, methscopolamine, and a combination of methscopolamine and scopolamine were evaluated in preventing physostigmine induced lethality in Swiss Webster mice. Low dose scopolamine was found to be highly effective in reversing high dose (3 X the LD100) physostigmine induced lethality, in contrast to methscopolamine, which was ineffective except in very high doses. A combination of scopolamine and methscopolamine was more effective than either drug alone.

Animals↗
PubMed1985

Effects of acute behavioral stress on plasma and cerebrospinal fluid ACTH and beta-endorphin in rhesus monkeys.

To elucidate the effect of acute behavioral stress on plasma and cerebrospinal fluid (CSF) concentrations of adrenocorticotropic hormone (ACTH) and beta-endorphin, rhesus monkeys were subjected to 30 min of confinement stress. Simultaneous plasma and CSF samples revealed no significant change in CSF ACTH or beta-endorphin up to 120 min after the onset of the stress despite significant elevations in plasma cortisol, ACTH, and beta-endorphin. It is suggested that acute behavioral stress does not alter CSF ACTH or beta-endorphin, and that this information may be clinically useful for future human studies of CSF ACTH and beta-endorphin in neuropsychiatric illnesses.

Acute Disease↗
PubMed1985

Effects of physostigmine on pulse, blood pressure, and serum epinephrine levels.

In this study, the infusion of physostigmine in 14 patients with affective disorder who were pretreated with methscopolamine caused significant and often profound increases in the patients' epinephrine levels, pulse rates, and blood pressure. Since physostigmine is being used experimentally in the treatment of elderly subjects who have Alzheimer's disease, these cardiovascular effects may have clinical importance.

Adult↗
PubMed1985

Depression and serotonin metabolism: rationale for neurotransmitter precursor treatment.

The authors review evidence suggesting that some depressed patients have disturbances in serotonin metabolism. Research supporting the serotonin hypothesis includes: cerebrospinal fluid studies; postmortem examination of neurotransmitters, their metabolites, and their receptors; platelet studies; neuropharmacologic data; neuroendocrine perturbations; and reports that serotonin precursor compounds (tryptophan and 5-hydroxytryptophan) may benefit some depressed patients. The authors conclude that better designed studies are needed to test whether serotonin precursor compounds have antidepressant properties.

5-Hydroxytryptophan↗
PubMed1985

The relationship of beta-endorphin and ACTH in the cerebrospinal fluid and plasma of adult surgical patients.

Cerebrospinal fluid and plasma beta-endorphin/beta-lipotropin immunoreactivity and adrenocorticotropin hormone were determined in simultaneously obtained samples from 25 healthy, adult surgical patients about to undergo spinal anesthesia using radioimmunoassay techniques. Cerebrospinal fluid adrenocorticotropin concentrations were significantly higher than those in plasma (25.76 +/- 2.11 fm/ml vs. 8.83 +/- 0.84 fm/ml), whereas beta-endorphin/beta-lipotropin concentrations in cerebrospinal fluid were significantly lower than those in plasma (6.60 +/- 0.43 fm/ml vs. 3.35 +/- 0.30 fm/ml). In cerebrospinal fluid, a significant positive correlation was found between beta-endorphin/beta-lipotropin and adrenocorticotropin (r = 0.64, p less than 0.01), whereas no such relationship could be demonstrated in plasma. This suggests that beta-endorphin/beta-lipotropin and adrenocorticotropin might enter the cerebrospinal fluid via a mechanism unrelated to their entry into plasma. This may have implications for the pharmacologic manipulation of these peptides within the central nervous system.

Adrenocorticotropic Hormone↗
PubMed1985

The dexamethasone suppression test and unipolar/bipolar distinctions.

In an attempt to validate several subtypes of affective disorders, 52 consecutive patients hospitalized at a clinical research center were comprehensively classified along several diagnostic and phenomenologic axes. Cortisol levels of each patient were evaluated at baseline and after the administration of 0.5 and 1.0 mg dexamethasone. None of the depressive subtypes responded significantly differently to the 1.0 mg dose. However, the bipolar subtype was associated with significantly different DST responses to the 0.5 mg dose. Patients with bipolar affective disorder, both manic and depressed, had higher postdexamethasone mean cortisol levels than all other groups. The results support the distinctiveness of the bipolar diagnosis.

Adolescent↗
PubMed1984

Central cholinergic stimulation causes adrenal epinephrine release.

Cholinergic drugs administered into the cerebral ventricles of animals selectively stimulate the adrenal medulla. However, the effects of central cholinergic stimulation on the sympathoadrenal system have not been studied in man. We stimulated central cholinergic activity in man by administering the cholinesterase inhibitor physostigmine to subjects pretreated with peripheral cholinergic blocking agents. A dose of 0.022 mg/kg physostigmine dramatically increased plasma epinephrine levels and slightly increased norepinephrine levels, which is consistent with selective adrenomedullary stimulation. A smaller dose of physostigmine increased epinephrine but did not alter norepinephrine levels. Subjects had increased pulse rates and blood pressures, and felt anxious while they had high plasma epinephrine levels.

Adrenal Medulla↗