Biomedical subjects

T Schuermeyer

Publications and source records attributed to T Schuermeyer.

4 recordsLinked to original sources

PubMed1990

Physiological regulation of circadian and pulsatile thyrotropin secretion in normal man and woman.

The circadian and pulsatile TSH secretion profiles were investigated in 5 females at the time of menstruation and 21 healthy males by sampling blood every 10 min for 24 h. Computer-assisted analysis, i.e. the Cluster and Desade programs, revealed means of 9.9 +/- 1.7 (Cluster) and 11.4 +/- 3.9 (Desade) pulses/24 h. More than 50% of the TSH pulses were detected between 2000-0400 h. Male and female subjects showed no significant difference in the basal mean and pulsatile secretion of TSH or in the TSH response to TRH (200 micrograms). Repetition of the TSH secretion analysis in 4 healthy subjects after 1, 2, and 6 months (2 subjects) revealed a significantly better cross-correlation within than between individuals (P less than 0.0001). We modulate the circadian TSH secretion pattern by acute sleep withdrawal or prolonged sleep after a night of sleep withdrawal in six healthy male volunteers. Sleep withdrawal augmented the nightly TSH secretion (mean serum TSH, 2.1 +/- 1.3 mU/L; mean TSH in sleep, 1.3 +/- 0.5 mU/L; P less than 0.05), whereas sleep after sleep withdrawal almost completely suppressed the circadian variation (mean TSH, 1.1 +/- 0.7 mU/L; P less than 0.01). This modulation is due to a significant decrease in pulse amplitude, but not to an alteration in the frequency or temporal distribution of TSH pulses.

Adult↗

PubMed1990

Circadian and pulsatile TSH secretion under physiological and pathophysiological conditions.

In addition to the well known circadian rhythm of TSH secretion a pulsatile pattern of release has been shown. Analysis of the pulsatile release by different computer-assisted methods revealed systematic differences in the number and distribution of TSH pulses. Using the same approximation of false positive pulses (less than 1%) in any of the 21 healthy male volunteers tested a lower number of pulses was found by the Pulsar method (mean 5.1 +/- 2.0/24 h) than by the Cluster (10.6 +/- 1.8) or the DESADE program (13.6 +/- 4.6). The results of the Cluster and Desade analysis fit well to that of Fourier transformation which revealed a dominant frequency at 160 min. In addition dominant frequencies in comparison to a noise series were found at 24 h and at 33 min. Analysis of the data in 8 h segments between 2000 and 0400 h, 0400 and 1200 h and 1200 and 2000 h by Desade and cluster revealed that app. 50% of pulses occurred between 2000 and 0400 h, suggesting an important role of pulsatile TSH release in the generation of the circadian TSH rhythm. In 3 patients with TSH-induced hyperthyroidism the circadian and pulsatile pattern of TSH secretion was similar to that in healthy controls. In contrast, in a patient with a TSH producing pituitary tumor the circadian variation of TSH secretion was abolished. Patients with a non-toxic goitre revealed a significantly lower mean TSH serum level as the control group of healthy subjects. The number of TSH pulses was slightly but significantly lower when analyzed by the DESADE program but not when analyzed with any other method.

Adult↗

PubMed1989

The role of glucocorticoids in the regulation of thyrotropin.

The potentially inhibitory action of endogenous or exogenous synthetic glucocorticoids on TSH secretion was investigated. Pulsatile and circadian TSH and cortisol rhythms were measured in healthy subjects (12 rhythms), but no correlation between the hormones could be detected. Acute stimulation of endogenous cortisol secretion by CRH tests (1 microgram/kg of ovine CRH) at 20.00 h in 9 healthy volunteers did not significantly alter the nightly increase in TSH. Chronic elevation of endogenous cortisol serum levels in patients with Cushing's disease revealed a heterogeneous pattern. In 2 patients serum TSH and thyroid hormone levels showed a normal 24-h rhythm, whereas the other 2 patients had low TSH serum levels. Acute treatment of 9 healthy volunteers with 0.5, 1 or 2 mg dexamethasone po at 23.00 h resulted in a significant dose-dependent suppression of mean basal TSH levels 9h later. Treatment with 30 mg of prednisone for 1 week in 7 patients with Crohn's disease did not influence basal TSH. The TSH response to TRH was only temporarily suppressed on day 3, but not on day 7 of treatment. The results suggest than under physiological conditions glucocorticoids have no regulatory influence on pulsatile and circadian TSH secretion.

Adult↗

PubMed1985

Corticotropin releasing factor: basic studies and clinical applications.

Corticotropin releasing factor (CRF) is a newly sequenced peptide first isolated from sheep hypothalami and thought to be an important modulator of both the pituitary-adrenal axis and the sympathetic nervous system. We administered intravenous, intramuscular, and intracerebroventricular CRH to non-human primates and measured plasma ACTH, beta endorphin, cortisol, GH and PRL responses to CRF. In addition, we determined the pharmacokinetic properties of I125 in these primates. We administered CRF as an intravenous bolus or as a continuous infusion to normal volunteers and as an intravenous bolus to patients with disorders of the hypothalamic-pituitary-adrenal axis, such as Cushing's syndrome and adrenal insufficiency, and patients with endogenous depression and mild hypercortisolism, and assessed their plasma ACTH, cortisol, GH and PRL responses. In addition, we determined the pharmacokinetic properties of CRF in man by measuring CRF immunoreactivity in plasma. CRF given intravenously to primates or man is a slowly metabolized, long-acting, secretagogue of ACTH, beta-endorphin and cortisol. When given intracerebroventricularly to primates it stimulates the hypothalamic-pituitary-adrenal axis without escaping into the plasma and it is actively cleared in the CNS. It does not cross the blood brain barrier appreciably when given intravenously. CRF given to primates and men as an intravenous continuous infusion has only mild ACTH stimulating effects and this may be due to an intact cortisol negative feedback system. Finally, CRF causes characteristic plasma hormone responses in patients with Cushing's disease, adrenal insufficiency and depression.

Adrenal Insufficiency↗