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Biomedical subjects

L Vanhaelst

Publications and source records attributed to L Vanhaelst.

At least 19 recordsLinked to original sources
PubMed1992

Differential dopamine-induced prolactin mRNA levels in various prolactin-secreting cell (sub)populations.

We have examined the effects of dopamine on prolactin gene expression using quantitative in-situ hybridization histochemistry in different pituitary cell (sub)populations separated according to their density on a discontinuous Percoll gradient. Administration of dopamine resulted in a drastic reduction in hybridization of 35S-labelled DNA probe complementary to prolactin mRNA in total pituitary cells and in lactotrophs with low density. In contrast, dopamine significantly stimulated mRNA accumulation in prolactin-secreting cells with high density compared with other cell layers. The combined use of Percoll gradient and quantitative in-situ hybridization is a valuable and sensitive method with which to examine prolactin-secreting cell response to a given stimulation. Prolactin-secreting cells with high and low density clearly show functional heterogeneity in their response to dopamine.

Animals↗
PubMed1991

Pharmacokinetics of intravenous and oral chlordesmethyldiazepam in patients on regular haemodialysis.

The pharmacokinetics of a single 2 mg IV dose of chlordesmethyldiazepam has been studied in 11 patients with renal failure on regular haemodialysis and in 11 age-matched healthy controls. The kinetics was also examined after a single 2 mg oral dose in 6 of the 11 renal failure patients. After intravenous administration the kinetics of total chlordesmethyldiazepam in renal patients and controls were the same. The unbound fraction of the drug in renal patients was higher (5.5%) than in controls (2.9%). Correction for differences in protein binding revealed a reduced apparent volume of distribution (47 vs. 140 l.kg-1) and a reduced clearance (5.0 vs. 10.5 ml.min-1.kg-1) in the patients. The systemic availability of oral chlordesmethyldiazepam was good (82%) despite a relatively slow absorption rate.

Administration, Oral↗
PubMed1991

Cyclical Cushing's disease. A case report.

A 41-year-old man with clinical Cushing's syndrome and intermittent central ACTH hypersecretion for a period of 9 1/2 years follow-up is described. Episodes of biochemical and clinical remission alternated with periods of florid Cushing's disease, characterized by circadian hyperpulsatile ACTH and cortisol secretion. Responses to metyrapone and inhibition of ACTH and cortisol hypersecretion after high dose dexamethasone during active phases of the disease favored a central origin of ACTH hypersecretion, confirmed by simultaneous bilateral venous sampling of the sinus petrosus inferior. Prolonged clinical remission followed near total anterior hypophysectomy. However, on anatomopathological examination of the pituitary neither corticotroph cell hyperplasia nor a microadenoma could be documented. The possibility of a functional ACTH hypersecretion is discussed.

Adrenal Glands↗
PubMed1991

Interleukin-1, interleukin-6: messengers in the neuroendocrine immune system?

Recent findings indicate that interleukin-1 (IL-1) and interleukin-6 (IL-6), cytokines secreted by immunologically activated monocytes and macrophages modulate neuroendocrine function. The site of production (centrally, peripherally), the site of action and the physiological significance of IL-1 and IL-6 as "classical hormones" are questioned.

Adrenocorticotropic Hormone↗
PubMed1991

Identification of a D1 dopamine receptor, not linked to adenylate cyclase, on lactotroph cells.

1. We studied the lactotroph cells of the rat by both in vivo and in vitro pharmacological techniques for the presence of D1-receptors. Both approaches revealed the presence of D2-receptor, stimulated by quinpirole (resulting in an inhibition of prolactin secretion) and blocked by domperidone. 2. Administration of fenoldopam, the most selective D1-receptor agonist currently available, resulted in a dose-dependent decrease of prolactin secretion in vivo (after pretreatment with alpha-methyl-p-tyrosine) and in vitro (cultured pituitary cells). This increase was dose-dependently blocked by the selective D1-receptor antagonist, SCH 23390, and although the effect of fenoldopam was less than that obtained by D2-receptor stimulation, these data suggest that a D1-receptor also controls prolactin secretion. 3. In order to detect the location of these dopamine receptors, autoradiographic studies were performed by use of [3H]-SCH 23390 and [3H]-spiperone as markers for D1- and D2-receptors, respectively. Specific binding sites for [3H]-SCH 23390 were demonstrated. Fenoldopam dose-dependently reduced [3H]-SCH 23390 binding, but had no effect on [3H]-spiperone binding. Immunocytochemical labelling of prolactin cells after incubation with [3H]-SCH 23390 revealed that the granulae and hence, D1 binding sites were present on the lactotroph cells. 4. Radioligand binding studies performed on membranes from anterior pituitary cells revealed the presence of the D2-receptor (54 fmol mg-1 protein) with a Kd of 0.58 nM for [3H]-spiperone, but failed to detect D1-receptors. 5. Finally, we studied the effect of dopamine and of fenoldopam on the adenosine 3':5'-cyclic monophosphate (cyclic AMP) content of anterior pituitary cells. Although cyclic AMP increased upon prostacyclin administration, indicating an intact adenylate cyclase system, fenoldopam failed to increase the cyclic AMP production. 6. It is tempting to speculate that fenoldopam reduces prolactin secretion through interaction with a non-cyclase-linked D1-receptor on the lactotroph cells.

Adenylyl Cyclases↗
PubMed1990

Development of monoaminergic neurotransmitters in fetal and postnatal rat brain: analysis by HPLC with electrochemical detection.

The monoamines dopamine, norepinephrine, epinephrine, and serotonin and their major metabolites 3,4-dihydroxyphenylacetic acid, homovanillic acid, 3-methoxy-4-hydroxyphenylethylene glycol, and 5-hydroxyindoleacetic acid were measured in the CNS of the rat during development from fetal day 18 to young adult. The catecholamines, serotonin, and their major metabolites remained low during fetal life. Concentrations measured in total brain started to increase around birth till the end of the fourth week of life after which steady-state levels were measured. Our results suggest that although monoamine systems are already morphologically well developed during late gestational life, they probably become a significant functional system only around birth and early postnatal life.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Prolactin response to TRH in diabetic ketoacidosis.

The prolactin response to 200 microgram thyrotropin-releasing hormone (TRH) IV was studied in seven patients with diabetic ketoacidosis, at the start of the treatment, and again, in the same patients, five days after recovery, when the diabetes was well controlled. Normal basal prolactin concentrations and prolactin responses to TRH were found in both situations. There was no correlation between basal prolactin concentrations, or magnitude of prolactin responses to TRH, and any of the metabolic variables measured. These findings do no suggest a role for prolactin in the development of diabetic ketoacidosis.

Adult↗
PubMed1979

Effect of cyproheptadine on thyrotrophin and prolactin secretion in normal man.

In order to investigate the effect of cyproheptadine, a compound with antiserotoninergic activity, on the secretion of thyrotrophin (TSH) and prolactin (PRL), the nocturnal secretory patterns of these hormones have been studied in 4 normal men in the basal state and after an oral treatment with the drug. In addition, the TSH and PRL responses to TRH of 6 women were compared in the basal conditions and after cyproheptadine treatment. The TSH nocturnal secretion was slightly modified by drug treatment. The response to TRH as well as the basal levels were comparable in the treated and non-treated subjects. In contrast, the PRL secretion measured through the nocturnal investigation was significantly inhibited by cyproheptadine administration as were the PRL basal levels in the TRH test. The PRL response to TRH was comparable in both situations.

Adult↗
PubMed1978

Pituitary-thyroid axis during short term, mild and severe, iodine depletion in the rat.

To investigate the most early events occurring during the adaptation of the pituitary-thyroid axis to iodine depletion, two rat populations were submitted to 4 week low iodine regimens of different severity. The variations of the following parameters were studied: pituitary thyrotropin (TSH) concentration, serum thyroxine (T4), triiodothyronine (T3) and TSH, thyroid weight and thyroid iodine concentration. In the first population, mildly iodine depleted, serum and pituitary TSH remained unchanged. The weight of the thyroid increased by the 12th day. Serum T4 dropped by the 26th day. Serum T3 tended to increase during the whole observation period. In the second population, more severely iodine depleted, the increase in thyroid weight appeared by the 4th day. Serum T3 increased from day 13 to day 20, then returned to normal. Serum TSH increased and serum T4 decreased by the 20th day. These results suggest that, in the adaptation to iodine deficiency in the rat, autonomous thyroid regulatory mechanisms play a major role at the onset of goiter growth. On the other hand, most likely a combined effect of serum T3 and T4 triggers variations in pituitary TSH secretion.

Animals↗
PubMed1978

A low T3 syndrome in diabetic ketoacidosis.

The pituitary-thyroid axis was investigated in nineteen euthyroid patients with severe diabetic ketoacidosis. A 'low T3 syndrome' was found, with the following characteristics: lowered serum concentrations of triiodothyronine (T3), increased reverse triiodothyronine (rT3), slightly low thyroxine (T4), normal thyrotrophin (TSH), slightly increased triiodothyronine uptake (RT3U) values, and a blunted TSH response to thyrotrophin-releasing hormone (TRH). These disturbances in thyroid-function tests required several days good control of the diabetes to be corrected, at least partially. The data suggest the presence of an abnormal extrathyroidal T4 metabolism as well as a pituitary defect. Caution is recommended in the interpretation of thyroid-function tests during and several days after the treatment of diabetic ketoacidosis.

Adult↗
PubMed1978

Acute endocrine profile of sulpiride in the human.

Normal men and normally menstruating women received i.m. injections of 0.1 to 4.0 mg/kg sulpiride. This psychotropic drug induced a very rapid (already significant after 5 minutes) and sustained (still significant after 7 hours) elevation of prolactin (PRL) concentrations in all subjects with no consistent modification of LH and FSH. After injection of 4.0 mg/kg, there was similarly no modification of mean TSH concentrations in the women tested in the luteal phase, as well as of mean GH levels in men. Sulpiride prevented the inhibitory effect on PRL levels of 500 mg levodopa, administered orally simultaneously; levodopa administered 2 hours prior to sulpiride failed to counteract the PRL-stimulatory effect of sulpiride. Under chronic sulpiride-induced hyperprolactinaemia, levodopa exhibited however a very slight inhibitory effect on PRL concentrations. These data are in agreement with the hypothesis that sulpiride acts mainly at the pituitary level by blocking dopamine receptors of the lactotropes and support the concept that the menstrual cycle perturbations observed under chronic sulpiride administration result from hyperprolactinaemia itself or from a mechanism quite similar to that by which sulpiride induces hyperprolactinaemia.

Adolescent↗
PubMed1978

Thyrotrophin, prolactin and growth hormone responses to TRH in barbiturate coma and in depression.

The effects of 200 microgram thyrotrophin-releasing hormone (TRH) i.v. on thyrotrophin (TSH), prolactin (PRL), growth hormone (GH) and triiodothyronine (T3) were studied in eight patients with barbiturate coma due to attempted suicide, in the same patients after recovery, in eight depressive patients and in eight normal controls. The patients with barbiturate coma presented normal basal TSH and PRL, elevated basal GH and normal PRL but blunted TSH responses to TRH; their GH concentrations varied widely without consistent relation to TRH administration. The same patients after recovery from coma presented normal TSH and PRL, slightly elevated basal GH, and normal PRL but blunted TSH responses to TRH; in four of these patients, a clear-cut rise in GH (i.e. more than 10 ng/ml) occurred after TRH administration. The depressive patients presented normal basal TSH and PRL, slightly elevated basal GH, and normal PRL but blunted TSH responses to TRH; in four of these patients, a moderated rise in GH (less than 10 ng/ml) occurred after TRH administration. The increment in T3 concentrations 120 min after TRH was found reduced in the comatose patients only. Basal cortisol was measured in all the subjects and found elevated in the comatose patients only. It is concluded that the abnormal TSH and GH responses to TRH observed in patients with barbiturate coma are more likely related to depressive illness than to an effect of barbiturates at the pituitary level. Barbiturates might affect thyroid secretion.

Adolescent↗
PubMed1977

Asymptomatic autoimmune thyroiditis and coronary heart-disease. Cross-sectional and prospective studies.

Cross sectional and prospective surveys of thyroid autoimmunity have been performed in two cohorts of men, 280 living in west Finland and 269 in east Finland. In both populations, aged 50 to 69 years at the first survey, risk factors for coronary heart-disease (C.H.D.) were common. The incidence of C.H.D. was shown to be related to the presence of thyroid antibodies. The results of the cross-sectional studies were not conclusive. The five-year follow-up study emphasised that in both areas asymptomatic thyroid autoimmunity, independently of other known risk factors, was a predictor of subsequent development of C.H.D. The importance of asymptomatic autoimmune thyroid-itis as a risk factor for C.H.D. increases with age.

Aged↗
PubMed1976

Pituitary and extrapituitary effects of somatostatin in normal man.

The effects of synthetic linear somatostatin on basal circulating levels on several pituitary and pancreatic hormones, and of glucose and free fatty acids (FFA) were studied in 6 normal men after an overnight fast. A priming intravenous infusion of 250 mug of somatostatin in 18 sec was followed by a constant infusion of 500 mug over a period of 60 min. A decrease in plasma values of GH, prolactin, TSH, insulin and glucagon and in blood glucose was observed during somatostatin infusion, while FFA levels increased progressively. Plasma IRI and blood glucose increased rapidly when the somatostatin infusion was stopped, while FFA decreased progressively; GH, prolactin, TSH and glucagon remained low as compared to basal levels for one hour after the end of the infusion, i.e. until the end of the experiment. A slight but significant increase of LH and ACTH was observed after the end of the infusion.

Adrenocorticotropic Hormone↗
PubMed1976

Paradoxical modulation of thyrotrope responsiveness to TRH during the treatment of thyrotoxic patients: apparent absence of feed-back regulation.

Eight patients with active thyrotoxicosis have been followed up to one year after the onset of antithyroid treatment. At different time intervals during the investigation period, TRH tests were performed and total T4 and T3 basal levels were measured. The TRH-induced TSH release was delayed in all patients in spite of a normalization of the circulating levels of thyroid hormones. The delay varied according to the patients and lasted, in some cases, for as long as 24 weeks after the normalization of the thyroid hormone levels. Administration of thyroid hormones, together with methimazole, did not seem to prevent the pituitary thyrotropes responsiveness; moreover, it did not provoke an inhibition of the TRH-induced TSH release once the thyrotropes reactivity was fully restored. The feed-back mechanism does not seem to be the main modulator of the pituitary responsiveness to TRH in these circumstances.

Adolescent↗
PubMed1976

Pituitary-thyroid axis reaction after myocardial infarction.

Within the first 36 hours following myocardial infarction, serum total thyroxine (T4) levels were supranormal in most cases in contrast to normal thyrotropin values. After one week, T4 levels dropped to normal while TSH values rose significantly. These findings suggest that, in the acute phase of myocardial infarction, the secretion of thyroid hormones is increased, thereby inhibiting the pituitary thyrotropes. The stimulation of thyroid secretion might be due to the high levels of blood catecholamines generally found in patients with myocardial infarction.

Aged↗