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Biomedical subjects

J L Rausch

Publications and source records attributed to J L Rausch.

33 records · Page 2Linked to original sources
PubMed1988

Platelet serotonin transport after a single ECT.

Platelet 5-HT uptake was examined in six depressed patients before and after a single electroconvulsive treatment and compared with six age- and sex-matched controls. The depressed patients had a significantly (P less than 0.05) lower Vmax of platelet 5-HT uptake prior to ECT (22.9 +/- 7.6 pm/2 x 10 platelets) than did control subjects (37.5 +/- 9.1 SEM). After a single ECT treatment, the Vmax significantly (P less than 0.05) increased to levels (34.6 +/- 10.1)no longer significantly different from control. The results are compared with recent data from depressed patients indicating that low baseline levels of platelet imipramine binding increase after ECT treatment.

Adult↗
PubMed1987

Measurement of ACTH and prolactin in the dexamethasone suppression test.

Plasma concentrations of ACTH and prolactin were measured in psychiatric inpatients at 8 a.m. and 4 p.m. before and after the standard 1 mg overnight Dexamethasone Suppression Test (DST). Plasma concentrations of cortisol were measured at 8 a.m. and 4 p.m., and 11 p.m. before and after 1 mg dexamethasone. Dexamethasone suppressed plasma concentrations of ACTH, prolactin and cortisol in the subject group as a whole. "Cut Points" obtained using Fisher's Exact Test identified plasma ACTH values at 8 a.m. baseline, 4 p.m. baseline and 8 a.m. post-dexamethasone and plasma prolactin values at all four times that significantly differentiated patients with bipolar depressive disorder and major depressive disorder from other psychiatric patients. There were no cut points found at any of the six times for plasma levels of cortisol that significantly differentiated between these two diagnostic groups. Of interest in this subject population, basal (pre-dexamethasone) plasma concentrations were of more diagnostic information than post-dexamethasone values. These pilot findings suggest that monitoring plasma prolactin and ACTH concentrations before and after dexamethasone might increase the sensitivity and specificity of this laboratory test for depression.

Adrenocorticotropic Hormone↗
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↗
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

Olfactory precipitants of flashbacks in posttraumatic stress disorder: case reports.

The phenomenon of vivid flashbacks elicited by olfactory stimuli is described in two combat veterans with posttraumatic stress disorder (PTSD). Although many sensory and cognitive cues can elicit flashback phenomena, smell has distinctive characteristics that make evocation of vivid olfactory memories particularly likely. It is recommended that clinicians inquire specifically about olfactory precipitants when evaluating combat veterans disabled by PTSD flashbacks.

Adult↗
PubMed1984

Complete heart block following a single dose of trazodone.

Forty minutes after receiving a single starting dose of trazodone, a patient developed complete heart block. The case illustrates that, despite the results of earlier studies, trazodone's effect on cardiac conduction may be severe in individuals at risk for conduction delay.

Aged↗
PubMedDate not supplied

Atenolol treatment of late luteal phase dysphoric disorder.

Activation of the renin-angiotensin-aldosterone system has been hypothesized as a potential pathophysiological factor in premenstrual tension syndrome (PMS). Atenolol is a predominate beta 1-blocker which can decrease plasma renin activity and inhibit the urinary excretion of aldosterone. Sixteen women meeting provisional diagnoses of late luteal phase dysphoric disorder were treated for symptoms of PMS with atenolol (50 mg once daily) in a randomized placebo-crossover double-blind design. The data indicated significant improvements on the irritability, vigor, elation, and friendliness scores in response to atenolol compared to placebo. Significant changes were not found for several other ratings scales, indicating that atenolol improved only selected symptoms in the group as a whole. However, the women who had premenstrual tension symptoms for more than 5 years (n = 8) were improved on most of the rating scales. Atenolol decreased premenstrual plasma aldosterone to a limited extent. There was also a trend in the data toward higher luteal progesterone levels during the month subjects took atenolol. Plasma renin activity and aldosterone correlated with estrogen and progesterone levels during the placebo month but not during the active month.

Adult↗
PubMedDate not supplied

Correlated cholinomimetic-stimulated beta-endorphin and prolactin release in humans.

Previous studies, both in animals and humans, have demonstrated that the intravenous or intraventricular administration of endogenous opioids and opiates produce dose dependent increases in plasma concentrations of prolactin. Notably, in humans, intravenous infusion of centrally active cholinomimetic drugs, such as physostigmine or arecoline, may produce significant increases in plasma concentrations of prolactin and beta-endorphin immunoreactivity. In three separate studies, conducted collaboratively between the National Institute of Mental Health and the University of California at San Diego, physostigmine and arecoline associated increases in plasma concentrations of beta-endorphin immunoreactivity were highly correlated with increases in plasma prolactin concentrations. These results are of interest because centrally active cholinomimetic drugs have been variously reported either to have no effect, to increase, or to inhibit anterior pituitary prolactin release. We propose that cholinergic stimulation of hypothalamic beta-endorphin may represent an interesting example of peptidergic modulation of primary neurochemical effects on hypothalamic-pituitary hormonal regulation.

Endorphins↗
PubMedDate not supplied

Hypothalamic-pituitary-adrenal regulation, neurotransmitters and affective disorders.

Considerable evidence has accumulated indicating that alterations in neurotransmitters may play a role in the etiology of affective disorders on the one hand, and in the regulation of the limbic-hypothalamic-pituitary-adrenal axis (LHPA) on the other. Acetylcholine, norepinephrine, serotonin, GABA, the opioid polypeptides and dopamine have all been implicated in both phenomena. Although some contradictory evidence exists, norepinephrine, opioids, and GABA appear inhibitory, and serotonin and acetylcholine appear excitatory of the LHPA axis. In a correlative study, non-suppression of cortisol by dexamethasone correlated positively and significantly with methylphenidate-induced euphoric and antidepressant responses, and methadone induced growth hormone responses, possibly suggesting catecholamine and opioid receptor hypersensitivity. Although the overall effects of the cholinomimetic, physostigmine, did not correlate with dexamethasone non-suppression, strong positive correlations were found in a subgroup, consisting of affective disorder patients, between non-suppression of cortisol by dexamethasone and the physostigmine response, suggesting cholinergic hypersensitivity in the non-suppressing subjects.

Alcoholism↗