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Biomedical subjects

T Ranta

Publications and source records attributed to T Ranta.

At least 109 records · Page 6Linked to original sources
PubMed1976

Hyperprolactinaemia and luteal insufficiency.

Prolactin interferes with the function of the corpus luteum, as was demonstrated by repeatedly finding a short luteal phase in the ovulatory cycles of two hyperprolactinaemic women after prolactin supression by bromocriptine had been discontinued. In hyperprolactinaemic ovulatory cycles excretion of pregnanediol in urine was less and plasma-progesterone concentrations were lower than in normo-prolactinaemic cycles. When the amenorrhoea-galactorrhoea syndrome recurred the symptoms appeared in the following order: (1) serum-prolactin increased and the luteal phase became shorter; (2) galactorrhoea appeared; (3) ovulation was missed; (4) menstruation was missed. All these abnormalities may be treated by prolactin suppression, but the effect of treatment does not persist for long after bromocriptine administration ceases.

Adult↗
PubMed1976

Choriocarcinoma: expression of tumor- and trophoblast-associated antigens in patients with low chorionic gonadotropin excretion.

The circulating levels of four tumor- or trophoblast-associated antigens were measured by specific radioimmunoassays in 11 patients with gestational choriocarcinoma. The estimations were carried out at the time when the urinary gonadotropin (hCG) excretion was low or negligible. Gonadotropin, measured as the hCG beta-subunit, was detected in serum of three patients, one of whom also showed a slightly raised level of carcinoembryonic antigen (CEA). All patients had normal serum alpha-fetoprotein (AFP) levels and no trace of human placental lactogen could be demonstrated. Repeat estimation after treatment of patients with raised levels showed a disappearance or a marked decrease of the circulating hCG levels and a return to normal of the elevated serum CEA level. The results show that although CEA levels may occasionally be elevated new information can hardly be expected from markers other than hCG when one is monitoring response to treatment, but AFP may have potential significance in the distinction between pregnancy and a trophoblastic disease. The circulating levels of hCG are of vital importance in the monitoring of choriocarcinoma patients who appear to be in remission by the conventional analysis of urinary hCG excretion.

Adult↗
PubMed1976

Anesthetics and thyrotropin secretion in the rat.

The effects of seven anesthetics (thiopentone, 50 mg/kg ip; pentobarbitone, 50 mg/kg ip; chloral hydrate, 300 mg/kg ip; urethane, 1,5 g/kg, 1/2ip, 1/2sc; ether; methoxyflurane, 1,5%; halothane, 2%) on basal serum TSH concentrations and on the cold-induced as well as the TRH-induced TSH responses were studied in Sprague-Dawley rats. The basal TSH level in female rats were decreased by ether and halothane at 30 min and somewhat increased by pentobarbitone and chloral hydrate. The cold-induced (4C, 30-60 min) TSH response of the warm-adapted male rats (30 C, 7 days) was decreased by all of the anesthetics studied, but the effect of pentobarbitone was not significant. The TRH-induced (50 ng iv) TSH response in female rats was totally abolished only by deep ether anesthesia but augmented by bariturates and chloral hydrate. It is concluded that all of the anesthetics studied can modify the secretion of TSH by their central effects. Ether in high concentration seems to be effective also at the pituitary level. The use of anesthetics may be a source of error when studying the neurotransmitter control of TSH-TRH secretion in the rat.

Anesthetics↗
PubMed1976

Prolactin and thyrotropin responses to thyrotropin-releasing hormone in patients with secondary amenorrhea: the effect of bromocriptine.

Prolactin (PRL) and thyrotropin (TSH) responses to a 200 mug intravenous thyrotropin-releasing hormone (TRH) bolus were measured by radioimmunoassay in 11 women with hyperprolactinemic amenorrhea and 9 with normoprolactinemic amenorrhea. In all cases, the tests were carried out under basal conditions and repeated during bromocriptine treatment. In women whose basal PRL level was normal; TRH caused a maximal PRL increment of 85 +/- 25.2 mug/l (mean +/- SE), while those women whose basal PRL level was raised showed a smaller increase (5.2 +/- 11.9 mug/l) (P=0.02). The peak levels were not significantly different in these two groups (95.0 +/- 26.7 and 134.6 +/- 35.9 mug/l) (P is greater than 0.1). During bromocriptine treatment, the raised PRL levels decreased in all cases, but levels over 30 mug/l remained in 3 patients, one of whom turned out to have a pituitary tumor. Prolactin responses to TRH were markedly inhibited in normoprolactinemic patients by the dose of bromocriptine used. The mean maximal net increase of PRL was 2.0 +/- 0.9 mug/l in normoprolactinemic patients and 11.0 +/- 8.1 mug/l in hyperprolactinemic patients taking bromocriptine. After TRH stimulation during bromocriptine, the peak PRL levels in hyperprolactinemic patients were higher (32.7 +/- 10.5 mug/l) than in normoprolactinemic patients (7.2 +/- 1.5 mug/l). Unlike what has been described for hypothyroid patients, the basal TSH level in euthyroid amenorrhea patients was not affected by bromocriptine, and we found that bromocriptine has no effect on the TRH-TSH response.

Adult↗
PubMed1976

Prolactin and testosterone: independent circulating levels in hyperprolactinemic and normoprolactinemic amenorrhea. The effect of prolactin suppression by bromocriptine.

In order to elucidate the pituitary regulation of the female testosterone secretion, we studied by radioimmunoassay the circulating prolactin (PRL) and testosterone-dihydrotestosterone (T-dT) levels in 12 hyperprolactinemic and 12 normoprolactinemic patients with secondary amenorrhea. After the basal levels had been recorded, each patient was given bromocriptine for two weeks, 2.5 mg twice daily, and repeat estimations of the PRL and T-dT levels were done. We found no significant difference in the basal T-dT levels between normoprolactinemic and hyperprolactinemic patients, and no significant correlation between the PRL and T-dT levels in either group. Although the PRL levels of the hyperprolactinemic patients were greatly suppressed by bromocriptine, the T-dT levels showed no systematic change. In normoprolactinemic patients, the T-dT concentrations were somewhat lower during bromocriptine treatment, but the difference from basal levels was not statistically significant (0.05 less than P less than 0.1). Our results suggest that in patients with secondary amenorrhea PRL does not interfere directly with T-dT secretion, or vice versa.

Adult↗
PubMed1976

Bromocriptine increases plasma estradiol-17 beta concentration in amenorrhea patients with normal serum prolactin.

In a series of 23 patients bromocriptine increased the plasma estradiol-17 beta level from 44.0 +/- 9.5 (mean +/- SE) to 144.1 +/- 31.8 pg/ml after 3 - 5 weeks' treatment (p less than 0.01). In normoprolactinemic patients (N = 12) the level increased from 59.6 +/- 16.3 to 186.5 +/- 50.5 pg/ml (p less than 0.05), and in hyperprolactinemic patients (N = 11) the corresponding values were 27.0 +/- 6.2 and 97.8 +/- 34.6 pg/ml (p less than 0.05). Bromocriptine treatment did not significantly alter the FSH and LH levels. The results suggest that bromocriptine treatment induces endocrine recovery also in patients whose clinical findings give no indication of prolactin suppression.

Amenorrhea↗
PubMed1976

Inhibition of mid-cycle gonadotrophin release in healthy women by pimozide and fusaric acid.

The effects of pimozide, a drug blocking dopamine receptors, and fusaric acid, an inhibitor of dopamine beta-hydroxylase, on mid-cycle release of FSH and LH were studied in 8 healthy women 20-25 years of age. None had used contraceptive drugs for the preceding 10 months. From the menstrual history and serum LH determinations during the normal cycle, mid-cycle gonadotrophin bursts were predicted for the following three cycles. Two days before and after the expected gonadotrophin surge were regarded as sufficient for the drug tests. Pimozide (initially 2 mg, then 1 mg/day) and fusaric acid (600 mg/day) were administered in a randomized cross-over study. The mid-cycle LH values were reduced from the control level of 56 +/- 10 mIU/ml (mean +/- SE) to 22 +/- 4 mIU/ml by pimozide (P less than 0.001) and to 17 +/- 5 mIU/ml by fusaric acid (P less than 0.001). The serum FSH level was 9 +/- 2 mIU/ml on the day of the LH surge and did not change significantly during treatment with either drug. The LH and FSH responses to synthetic LRF (100 mug iv) were not changed by pimozide or fusaric acid. The rise of basal temperature associated with ovulation was not affected by the drugs. These results suggest that suprapituitary noradrenergic and dopaminergic neurotransmitters are involved in the regulation of mid-cycle gonadotrophin secretion in women.

Adult↗
PubMed1976

Augmented secretion of TSH in response to TRH after pre-treatment with dexamethasone for six days in rats.

Serum TSH and corticosterone concentrations were measured in rats given TRH or exposed to short-term cold, as well as in intact rats, after pre-treatment with dexamethasone for six days at two different dose levels (25 and 250 mug/100 g body weight). Both doses increased the secretion of TSH in response to TRH whereas cold-induced TSH secretion was not modified by pre-treatment with dexamethasone. In intact rats serum TSH levels did not differ significantly from controls. In all experiments the steroid blocked ACTH secretion. It was also found that administration of TRH produced a rise in serum corticosterone concentrations. Our results support the view that dexamethasone given for six days facilitates TRH stimulation of the pituitary whilst simultaneously inhibiting the secretion of TRH in response to cold.

Adrenocorticotropic Hormone↗
PubMed1976

Biological effects of a new and potent progestagen. A clinical study.

The biological effects of a new synthetic progestagen, Org 2969 (13-ethyl-11-methylene-18,19-dinor-17 alpha-pregn-4-en-20-yn-17-ol) were studied in healthy normally menstruating women. Two of them were given 0.125 mg, five 0.060 mg and two 0.030 mg of Org 2969 daily on days 1-20 during one menstrual cycle. Serum levels of follicle stimulating hormone, luteinizing hormone, progesterone and oestradiol were analyzed on days 8-23 in order to evaluate the function of the hypophyseal-ovarian axis. The serum concentrations of aspartate amino transferase, alanine amino transferase, alkaline phosphatase, gamma glutamyl transpeptidase and bilirubin were determined to evaluate possible side effects on live function on days 8, 15 and 23. Serum cortisol was measured on days 8 and 23. The basal body temperature was recorded daily during the whole cycle, and endometrium biopsies were taken on days 21 or 22 of the cycle. All samples were taken similaryl during the treatment cycle and the preceding control cycle. According to the hormone determinations, all the treatment cycles were anovulatory except in one woman receiving the lowest dose. The treatment led to decreased spinnbarkeit, arborization and sperum penetration in the cervical mucus. Liver function tests and serum cortisol remained unchanged during the treatment.

Administration, Oral↗
PubMed1975

Raised serum prolactin levels in amenorrhoea.

Serum prolactin levels measured by specific radio-immunoassay were over 30 mug/l in seven out of 25 women with amenorrhoea and in eight women with the amenorrhoe-galactorrhoea syndrome. There was no apparent relationship between these levels and levels of follicle-stimulating hormone, luteinizing hormones, and thyroid-stimulating hormone. Bromocriptine caused a transient fall in the proclatin levels in six out of seven cases, and in three menstruation and ovulation were restored. Estimation of serum prolactin may become important in assessing the degree of hypothalamic-pituitary dysfunction in amenorrhoea, and it may help in identifying a subgroup of patients at risk of developing a pituitary tumour or patients who may respond to specific treatment.

Adult↗
PubMed1975

Neurotransmitter control of thyrotropin secretion in the rat.

In rats adapted to a +30 degrees C temperature for one week, transfer to a temperature of +4 degrees C increased immunoassay-able serum TSH from 150-300 ng/ml to 800-2000 ng/ml in 30 min. Since this response, as well as the level of serum TSH without stimulation, were decreased by reserpine, phentolamine, phenoxybenzamine, disulfiram and diethyldithiocarbamate, noradrenaline may be involved in the stimulation of TSH secretion. TRH-induced TSH increased was not blocked by reserpine. 1-Dopa, a noradrenaline precursor, decreased the TSH response to cold; alpha-methyl-p-tyrosine increased the TSH level. Apomorphine decreased the level of serum TSH and inhibited the response to cold. The possibility of a dopaminergic inhibitory factor released from the hypothalamus is discussed. 5-HT has possibly a role in the regulation of TSH secretion, since its precursor 5-HTP decreased the response to cold. No indication was found that acetylcholine is involved.

Acetylcholine↗
PubMed1975

Secretion of anterior pituitary hormones in man: effects of ethyl alcohol.

The possibility that previously described effects of ethyl alcohol on peripheral endocrine glands might be mediated via pituitary prompted this investigation on the effects of ethanol on anterior pituitary secretion. Nine healthy male subjects were given beverage containing ethanol (1.5 g/kg) or beverage alone per os in a randomized cross-over study and plasma ACTH, FSH, GH, LH and TSH were measured by specific radioimmunoassays up to 15 h and the urinary levels of adrenaline and noradrenaline by fluorometry. A combined LRF and TRF test was also carried out in similar series of experiments. During the whole experiment there were no significant differences in the plasma levels of ACTH, FSH and TSH or in the urinary levels of adrenaline and noradrenaline between ethanol treated and control subjects. Plasma FSH, LH and TSH responses to LRF and TRF stimulation were also similar in alcohol treated and control subjects. Plasma ACTH values were high (113-270 pg/ml) both in control and ethanol experiment suggesting that the subjects experienced apprehension toward the experiment. Plasma GH level exhibited a non-sleep related burst in the late evening (from 0.4 ng/ml at 6 p.m. to 3.1 ng/ml at 10 p.m., p less than 0.01). This increase was not seen after alcohol ingestion (p less than 0.01). Plasma LH levels were significantly lower after 6 and 13 h in alcohol treated subjects than in controls (65 vs. 106 ng/ml, p less than 0.01 and 74 vs. 121 ng/ml, p less than 0.05 respectively). Because ethanol had no effect on the resting level of plasma GH or on the LH response to LRF, WE SUggest that ethanol exerts these effects on a suprapituitary site.

Adrenocorticotropic Hormone↗
PubMed1975

Pulsatile secretion of ACTH, GH, LH and TSH in man.

Blood samples were taken every 4 min for 80 min from 5 healthy subjects. Plasma ACTH, GH, LH and TSH were estimated by radioimmunoassays. The mean peak intervals were 11, 12, 13 and 14 minutes respectively and mean peak amplitudes were 25 pg, 1.1 ng, 11 ng and 5.3 muU. Mean durations of ascending and descending limbs of the plasma patterns of these hormones were also measured. The timing of the different hormone peaks appeared to be independent.

Adrenocorticotropic Hormone↗
PubMed1975

Serum tri-iodothyronine, thyroxine, and thyrotrophin concentrations in newborns during the first 2 days of life.

The serum concentrations of tri-iodothyronine (T3), thyroxine (T4), and thyrotrophin (TSH) were measured in 10 term newborn infants between birth and the age of 2 days by radioimmunoassay. The mean concentration of T3 in maternal serum was 1.62 mug/l, and it increased from the low cord blood level of 0-63 mug/l to the peak value of 1-76 mug/l within the first 2 hours of life. Mean serum T4 concentrations increased from the cord blood level of 145 mug/l to the peak value of 205 mug/l within the first 24 hours of life. The postnatal increase of the mean serum TSH concentrations from the cord blood level of 5-7 mU/l to the peak value of 20-6 mU/l within 2 hours was similar to the increase of T3. These data confirm earlier reports which show that T3 secretion is low at birth and TSH secretion is stimulated strongly but transiently after birth, and that the low T3 secretion is rapidly normalized in 2 hours along with the TSH release. Because of these strong and rapid changes, we recommend screening of the function of the pituitary-thyroid axis in neonates after the age of 24 hours.

Adult↗
PubMed1975

Effect of dexamethasone on the secretion of thyrotropin in the rat: dose and time relations.

Serum TSH and corticosterone concentrations were measured in intact rats and in rats given TRH or exposed to short-term cold 3 h and 12 h after pretreatment with dexamethasone in various doses. Dexamethasone given 3 h before experiemtns significantly depressed both TRH- and cold-induced TSH responses at all dose levels. Dose of 25 pg/100 g body weight significantly depressed serum TSH concentration when given 3 h before the experiment. However, when given 12 h before the experiment the drug augmented TRH-induced TSH secretion, although the cold response was unaltered. In intact rats dexamethasone significantly depressed serum TSH concentration in doses of 250 and 500 mug/100 g body weight. In all experiments the steroid blocked ACTH secretion. These results support the view that the effect of dexamethasone on thyroid function is highly dependent on the time relations. A single large dose of dexamethasone has first an inhibitory effect at the pituitary level and then facilitates pituitary to TRH and at the same time inhibits secretion of TRH in response to cold.

Adrenocorticotropic Hormone↗