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Biomedical subjects

R L Trestman

Publications and source records attributed to R L Trestman.

33 records · Page 2Linked to original sources
PubMed1992

Noradrenergic responses to clonidine in acute and remitted depressed male patients.

To investigate noradrenergic function in depression, plasma 3-methoxy-4-hydroxyphenylglycol (MHPG), plasma norepinephrine (NE), mean arterial pressure (MAP), and heart rate responses to intravenous clonidine (2 micrograms/kg), an alpha 2-adrenergic agonist, were measured in 27 acutely depressed patients, 18 remitted depressed patients, and 27 normal control subjects; a placebo infusion was administered to a subgroup. Clonidine compared with placebo, over a 150-minute time course, decreased plasma NE, MAP, and heart rate, but not plasma MHPG, in the control subjects. Plasma MHPG, plasma NE, MAP, and heart rate at baseline or in response to clonidine and placebo over 150 minutes did not indicate any group differences. The only significant plasma MHPG response to clonidine in the normal control subjects occurred 60 minutes after the infusion. A significantly diminished plasma MHPG response to clonidine at 60 minutes was found in the acutely depressed group compared with the normal control subjects. These results suggest that peripheral inhibitory noradrenergic responses to clonidine are normal in depressed patients, while plasma MHPG responses to clonidine, which have a limited central contribution, appear to be a weak reflection of central noradrenergic function and appear insufficiently robust for a meaningful evaluation of hypothetical group differences in central inhibitory alpha 2-adrenergic activity in this population.

Acute Disease↗
PubMed1992

The growth hormone response to clonidine in acute and remitted depressed male patients.

The growth hormone (GH) response to clonidine was evaluated in 28 acutely depressed male patients, 17 remitted depressed patients, and 26 normal control subjects. The GH response to clonidine was blunted (delta less than 4 ng/ml) in a significantly increased proportion of both acute and remitted patients compared to control subjects. Covarying for age effects, the GH response to clonidine (as area-under-the-curve) was not significantly different between any of the three groups, but was significantly diminished in both the acute and remitted depressed patients who were ever hospitalized for an episode of depression, compared to control subjects. Six patients studied in both the acute and remitted states were blunted in both states. These findings could not be accounted for by other clinical and demographic variables including weight, time off antidepressants, severity of current depressive symptoms, and subtype of depression. These results raise the possibility that the blunted GH response to clonidine may represent a state-independent correlate of some forms of severe depression. Issues regarding the specificity and interpretation of this finding require further clarification.

Acute Disease↗
PubMed1991

Biochemical mechanisms of stress-induced impairment of rat T cell mitogenesis.

Splenic mononuclear cells isolated from rats exposed to two brief stressors (5 min of restraint or 2 min of footshock) showed a diminished response to the T cell mitogens, concanavalin A and phytohemagglutinin. Cells from these stressed animals also exhibited a diminished response to stimulation with the phorbol ester, tetradecanoylphorbol acetate (TPA), and/or the calcium ionophore, ionomycin. Since stimulation with these latter two agents mimics early signals generated by mitogen surface receptor binding including increased intracellular calcium and protein kinase C activation, the data indicate that stress-related defects in T cell proliferation occur at sites other than or in addition to these early events in cellular activation.

Analysis of Variance↗
PubMed1991

Adrenal steroid receptor activation in vivo and immune function.

Recent studies have indicated significant differences among immune and other tissues in in vivo adrenal steroid receptor activation after a given hormone exposure. Nevertheless, the relationship between in vivo receptor activation and functional measures of the immune response has not been determined. Type I and type II adrenal steroid receptor binding in conjunction with mitogen-induced T-cell proliferative responses were measured in the spleens of Sprague-Dawley rats that were administered various concentrations of dexamethasone (DEX). A linear relationship between type II receptor binding and splenocyte proliferation was found, with decreases in measurable type II receptors (indicating in vivo receptor activation) being highly correlated with decreases in immune function. There was no evidence of spare type II receptors. In vitro studies using the type II receptor antagonist RU 486 confirmed that the inhibitory effect of DEX on splenocyte proliferation was mediated via the type II receptor. These findings provide a foundation for future studies evaluating glucocorticoid effects on immune system function and suggest that evidence of in vivo receptor activation may be critical for predicting when and in which tissues adrenal steroid hormones may be capable of modulating the immune response.

Analysis of Variance↗
PubMed1990

Psychiatric perspectives of brain, behavior, and the immune system.

There is increasing evidence of reciprocal CNS-immune system interactions. The reaction of such processes to behavior and psychiatric disorders remains to be determined. It is not clear at this time if alterations in measures of the immune system associated with stress have clinical relevance, nor is there evidence that immune alterations are associated with the pathogenesis of psychiatric disorders. With the exciting advances in neurobiology, immunobiology, and biologic psychiatry, and with the availability of a wide range of methodologies, elucidation of the complexities of brain, behavior, and the immune system may be achieved.

Animals↗
PubMed1985

Hormonal and drug effects on the degradation of human myelin basic protein peptide 43-88 by alkaline proteolytic activity in the rat kidney.

The microsomal brush-border fraction of rat renal tissue contains enzymatic activity, optimally active at pH 9, that is capable of degrading human myelin basic protein (BP) peptide 43-88. In the present study, this degradation and the effect on it of selected drugs and hormones were examined further. Of the substances tested, 10(-2) M chloroquine and 10(-5) M ACTH 1-24 were found to be the most effective inhibitors followed by 10(-5) M ACTH 1-39; parathormone, glucagon and insulin were found to be inhibitors an order of magnitude weaker than ACTH 1-24. Hydrocortisone, dexamethasone, maleic acid and ACTH 4-10 were found to have minimal or no inhibitory effect on the peptide degrading activity. Gel filtration of the degradation products indicated that the rate of degradation of BP peptide 43-88 at pH 9 had been retarded by ACTH 1-24. These studies indicate that the clearance and catabolism of this peptide may be altered by available therapeutic agents.

Adrenocorticotropic Hormone↗