Plasma TSH Concentrations Research Articles

Measurement of TSH in plasma and pituitary of the rat by a radioimmunoassay utilizing bovine TSH: effect of thyroidectomy or thyroxine administration on plasma TSH levels.

A method for radioimmunoassay of bovine TSH has been developed which can be used to measure plasma TSH concentration in the rat and mouse and pituitary TSH concentration in the rat, beef, pig, mouse, sheep, rabbit and monkey. Hormonal specificity has been demonstrated by lack of interference in the assay by rat growth hormone and bovine LH. Preparations of rat FSH cross-react slightly in the assay system, an effect attributable to TSH contamination. Rat LH cross-reacts to a greater degree. The effect is due in part to TSH contamination but may also be due to true antigenic similarity between TSH and LH. The extent of cross-reactivity between LH and TSH is slight and does not interfere with the TSH specificity of the assay since plasma levels are not elevated in gonadectomized animals, and are not detectable in T4-treated animals. Using bioassayed rat pituitary extract as standard, normal (decapitate) plasma TSH in the male rat, 200–250 g body wt, was 47.3 ±7.2, 42.6 ±5.0 and 29.0 ±4.8 mU/100 ml in separat...

The effect of glucocorticoids on thyrotropin secretion

The effect of large doses of glucocorticoids on thyrotropin (TSH) secretion in normal and hypothyroid humans has been studied. Plasma TSH concentrations were measured before, during, and after treatment with dexamethasone given orally for 24-48 hr. In 17 patients with primary hypothyroidism, plasma TSH levels fell significantly during treatment to a mean of 54% of control (range 23-96%). Within 48 hr after the withdrawal of dexamethasone, TSH concentrations transiently increased above pretreatment values. The mean increase was to 156% of control (range 106-294). Similar changes, but of smaller magnitude, were observed in 15 normal subjects. Administration of single oral doses of dexamethasone and oral or intravenous doses of cortisol were followed by reduction of plasma TSH levels to 18-47% of control within 8-12 hr in eight hypothyroid patients. This fall also was followed by significant TSH rises above control values before they returned to the pretreatment levels. Mineralocorticoid administration was not followed by any changes in plasma TSH concentrations in three subjects.TSH responses to steroid were also studied in rats. In hypothyroid rats given dexamethasone intravenously, plasma TSH fell to 63% of control in 30-90 min and then returned to normal or above in 3-4 hr. Dexamethasone also reduced plasma TSH concentrations in normal rats but no rebound was observed in these animals. Dexamethasone did not block the increase in plasma TSH produced by thyrotropin releasing factor (TRF) administration in vivo. Neither basal nor TRF-mediated TSH release from hemipituitaries in vitro was reduced by dexamethasone or corticosterone. These studies indicate that glucocorticoids reduce TSH secretion and suggest that this effect occurs at a suprahypophyseal level.

Estimation of the secretion rate of thyrotropin in man.

The plasma concentration of a pituitary hormone is determined by the rate of secretion, degradation, and the volume of distribution of that hormone. Using a radioimmunoassay for human thyrotropin (TSH) and human TSH-(131)I, we have estimated the rates of degradation and distribution of TSH in man and calculated the rate of secretion. Either 0.5 or 5 mug of TSH-(131)I with specific activities of 1 to 50 muc per mug was administered intravenously to 12 euthyroid subjects. Serial determinations were made of TSH-(131)I, and the half-time of disappearance (t((1/2))) was thus estimated. The average t((1/2)) in euthyroid subjects was 53.9 minutes with a volume of distribution averaging 5.8% of body weight. The mean endogenous plasma TSH concentration was 1.8 mmug per ml (2.7 muU per ml in terms of the human TSH reference standard A). The mean total TSH pool, excluding the pituitary, was 5.8 mug (8.7 mU). From these data the mean secretion rate of TSH in euthyroid man was calculated to be 110.1 mug per day (165.2 mU). Similar data were estimated for 3 mildly hypothyroid patients. The t((1/2)) were 75.1, 97.1, and 83.6 minutes, with a mean of 85.3 minutes (1.6 times normal). The mean TSH pool was 58.1 mug (10 times normal). The secretion rate was 688.7 mug per day (1,033.1 mU). In other hypothyroid patients, plasma TSH levels ranging from 6 to 230 mmug per ml (9 to 345 muU) have been found. If similar half-times and a normal distribution volume are assumed, the secretion rate of TSH in hypothyroid patients can be estimated to range from about 260 to 15,350 mug per day (390 to 23,025 mU) or from about 2 to 307 times normal. Therefore, the elevated plasma TSH levels found in hypothyroidism are a result of both slower degradation and increase in rate of secretion.

Reversal of the inhibition of TSH secretion due to acute stress.

Chronic stress of minor intensity prevents the usual inhibition of TSH secretion induced by an acute stressing procedure. Chronic administration of reserpine reverses the usual inhibition of TSH secretion induced by acute stress, which is now followed by an elevation of plasma TSH concentration. Chronic stress leads to increased resting levels of plasma TSH. The studies reported here were conducted on rats with direct measurements of plasma TSH levels by bio-assay. (Endocrinology 80: 953, 1967)

Regulation of the pituitary-thyroid axis in man: relationship of TSH concentration to concentration of free and total thyroxine in plasma.

ABSTRACT To study thyroid-pituitary interrelationships in man, serial measurements of plasma thyrotropin (TSH), protein-bound iodine (PBI) and free thyroxine have been made in hypothyroid patients during therapy with L-thyroxine. In each patient, PBI and free thyroxine concentrations increased progressively during therapy. Conversely, initially elevated plasma TSH concentrations fell, ultimately becoming undetectable in all. Thus, a curvilinear relationship was found relating plasma TSH to both PBI and free thyroxine. At concentrations of free thyroxine below the normal, plasma TSH rises rapidly with small decrements in circulating thyroid hormone. Above this point, relatively smaller reductions in plasma TSH accompany similar increments in total or free thyroxine levels. The secretion of pituitary TSH appears to be finely regulated over a wide range of plasma thyroid hormone concentrations.

Lability of plasma TSH levels in the rat in response to nonspecific exteroceptive stimuli.

SummaryMild nonspecific exteroceptive stimuli such as handling, transferring from one room to another, and I.P. injections, lead to a rapid decrease of plasma TSH concentrations which become undetectable within 15 minutes following the beginning of the stressing procedure. There is evidence for a circadian rhythm of plasma TSH levels in opposite phases to those of the variations of plasma ACTH or corticosteroid variations. These observations are considered to be of importance to define resting levels of plasma TSH concentrations. For rats kept at 22°C ± 0.5, rapidly decapitated at 7:00 a.m., resting levels of circulating TSH are between 25–30 mU/100 ml plasma in this laboratory.

Increase of plasma TSH concentration following injection of purified hypothalamic TRF.

A purified preparation of TSH-releasing factor (TRF), specific activity 30 U/mg, of sheep hypothalamus origin, elevates the levels of circulating plasma TSH from 21 to 197 mU/100 ml in 3 min following intravenous injection in normal animals; even though less marked in amplitude, the same effect is seen in thyroidectomized animals. The material has no effect in hypophysectomized animals. (Endocrinology 77: 792, 1965)

ELECTRICAL STIMULATION OF THE HYPOTHALAMUS: SIMULTANEOUS EFFECTS ON THE PITUITARY-ADRENAL AND THYROID SYSTEMS OF THE RAT.

Electrical stimulation of various sites in the medial ventral hypothalami of adult female rats was done through chronically implanted electrodes in order to determine simultaneous effects on the pituitaryadrenal and thyroid systems. A series of stimulations (10 min daily, 4–9 days) delivered to preoptic, suprachiasmatic and anterior hypothalamic areas induced cytological activation of pars distalis basophils, markedly reduced pituitary thyrotrophin (TSH) stores, increased plasma TSH concentrations 4- to 5-fold, and resulted in histological stimulation of the thyroid gland. Comparable excitation of the posterior median eminence and arcuate nuclear regions of the tuberal hypothalamus produced effects of similar magnitude. The mere presence of electrodes in the hypothalamus without electrical stimulation had no significant effect on TSH secretion and histology of the thyroid, but caused adrenal hypertrophy and elevation of plasma corticosteroid levels in sham-stimulated rats. Excitation of the rostral or cau...

THYROTROPHIC HORMONE IN THE PLASMA AND ANTERIOR PITUITARY OF THE THYROIDECTOMIZED RAT.

SUMMARY The changes in plasma concentration and anterior pituitary content of thyrotrophic hormone (TSH) after thyroidectomy in the rat were followed by means of an in vitro assay method. A triphasic change in plasma TSH was demonstrated which consisted of a threefold rise by the 2nd day, a fall to the normal range by the 5th day, and a gradual rise from the 10th day, which continued for at least 6 weeks. The initial rise in plasma TSH was accompanied by a fall in the pituitary TSH store after 5 days to 7 % of the normal value; the store then remained low for the next 6 weeks. Thyroxine (as measured by protein-bound 131I) disappeared from the circulation after thyroidectomy at a rate compatible with the observed rate of rise of plasma TSH; 20 % remained after 2 days. The replacement of thyroid hormone by exogenous thyroxine in thyroidectomized rats resulted in 4 days in a decline in plasma TSH concentration to a subnormal value. During the next 3 days the blood level of TSH rose to 400 % of the control level. Thyroxine administration caused a large increase in the pituitary store of TSH. The results indicate that circulating thyroxine influences primarily the rate of release of TSH from the anterior pituitary, and that a slower effect on the synthesis of TSH may be indirect and secondary to changes in the TSH content of the pituitary gland.