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Biomedical subjects

E Finné

Publications and source records attributed to E Finné.

17 recordsLinked to original sources
PubMed1999

Calcitonin reserve in different stages of atrophic autoimmune thyroiditis.

The objective of this study was to determine the calcitonin (CT) hormone reserve in different severity of atrophic autoimmune thyroiditis (AAT). Forty-eight female patients with AAT were divided into four groups based on basal and peak thyrotropin (TSH) values (after oral thyrotropin-releasing hormone [TRH], free triiodothyronine (FT3) and free thyroxine (FT4) ranging from normal in group 1 to overt hypothyroidism in group 4. All had thyroid antibodies. The control group comprised euthyroid females of comparable age, without thyroid antibodies. Basal CT and CT response to calcium infusion (area under the curve) were investigated as parameters of CT reserve. Basal CT was lower in groups 2 to 4 of patients with AAT (compared to controls), but the difference was not significant. Stimulated CT levels were lower (p < 0.05) in all groups of patients compared to controls, with markedly reduced CT-secretory reserve in group 4. Thyroid antibody concentrations and, basal and postinfusion calcium levels were not significantly different among the various groups. In conclusion CT deficiency (especially stimulated values) occurs in AAT and is more severe in hypothyroid patients than in earlier stages of AAT.

Administration, Oral↗
PubMed1997

Effect of N omega-nitro-L-arginine methyl ester, a nitric oxide synthesis inhibitor, on stress- and morphine-induced prolactin release in male rats.

1. The effect of the nitric oxide synthesis inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) was investigated on stress- and morphine-induced prolactin (PRL) secretion in vivo in male rats, by use of a stress-free blood sampling and drug administration method by means of a permanent indwelling catheter in the right jugular vein. 2. Three doses of L-NAME were tested (1, 10 and 30 mg kg-1) and were given intraperitoneally one hour before blood sampling; control rats received saline. After the first blood sample, rats received an initial intravenous injection of morphine (3, 6 or 12 mg kg-1) or were subjected to immobilization stress. In the case of a morphine administration, rats received a second dose of morphine (3, 6 or 6 mg kg-1, respectively) 90 min later, when tolerance had developed, while rats subjected to immobilization stress received 6 mg kg-1 morphine 90 min after onset of stress. 3. L-NAME had no effect on basal plasma PRL concentration. However, it potentiated acute morphine-induced PRL secretion and attenuated the subsequent tolerance in a dose-dependent way. Immobilization stress-induced PRL secretion was inhibited dose-dependently by L-NAME, as was its subsequent tolerance to morphine; however, in this case, in a reversed dose-dependent way. 4. When the highest dose of morphine (12 mg kg-1) was combined with the highest dose of L-NAME pretreatment (30 mg kg-1), all rats showed a dramatic potentiation of the morphine-induced PRL rise compared to controls. Moreover, all of these rats died within 90 min after the administration of morphine. 5. These results show that NO plays a role in the acute opioid action on PRL release during stress as well as in the development of tolerance to the opioid effect, and some possible mechanisms are discussed.

Animals↗
PubMed1996

Modulating effect of the nootropic drug, piracetam on stress- and subsequent morphine-induced prolactin secretion in male rats.

1. The effect of the nootropic drug, piracetam on stress- and subsequent morphine-induced prolactin (PRL) secretion was investigated in vivo in male rats, by use of a stress-free blood sampling and drug administration method by means of a permanent indwelling catheter in the right jugular vein. 2. Four doses of piracetam were tested (20, 100, 200 and 400 mg kg-1), being given intraperitoneally 1 h before blood sampling; control rats received saline instead. After a first blood sample, rats were subjected to immobilization stress and received morphine, 6 mg kg-1, 90 min later. 3. Piracetam had no effect on basal plasma PRL concentration. 4. While in the non-piracetam-treated rats, stress produced a significant rise in plasma PRL concentration, in the piracetam-pretreated rats PRL peaks were attenuated, especially in the group given 100 mg kg-1 piracetam, where plasma PRL concentration was not significantly different from basal values. The dose-response relationship showed a U-shaped curve; the smallest dose had a minor inhibitory effect and the highest dose had no further effect on the PRL rise. 5. In unrestrained rats, morphine led to a significant elevation of plasma PRL concentration. After the application of immobilization stress it lost its ability to raise plasma PRL concentration in the control rats, but not in the piracetam-treated rats. This tolerance was overcome by piracetam in a significant manner but with a reversed dose-response curve; i.e. the smaller the dose of piracetam, the higher the subsequent morphine-induced PRL peak. 6. There is no simple explanation for the mechanism by which piracetam induces these contradictory effects. Interference with the excitatory amino acid system, which is also involved in opiate action, is proposed speculatively as a possible mediator of the effects of piracetam.

Animals↗
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

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

Analysis of the receptor specificity of tolerance induction in stress versus opioid-related prolactin secretion in rats.

The effects of restraint stress and opiates on prolactin secretion in male rats have been measured. Both induced a short-lived increase in prolactinaemia. Experimental evidence indicates that both opioids and restraint stress bring about their actions by the activation of opioid receptors. When restraint stress was followed by administration of the specific kappa-agonist bremazocine, a second prolactin peak was observed. In contrast, morphine (predominantly a mu-agonist) lost its prolactin-stimulating capacity when given after a period of restraint stress. This indicates cross-tolerance between restraint stress and morphine. Tolerance was overcome when the dose of morphine was doubled, and an increase in prolactin secretion could again be obtained. The cross-tolerance phenomenon argues that a common opioid receptor is involved in morphine- and restraint stress-stimulated prolactin release. In another set of experiments, in which morphine administration replaced restraint stress as a means of inducing tolerance, a second rise in prolactinaemia was seen only with bremazocine and not with a further administration of morphine. This suggests a morphine (mu) receptor-specific development of tolerance. Two consecutive administrations of bremazocine also produced tolerance, in this case for the kappa-receptor. This illustrates the rapid and receptor-specific development of tolerance for the prolactin-releasing capacity of opioid compounds.

Animals↗
PubMed1990

The growth hormone secretory response to fentanyl in rat: an involvement of mu type receptors.

Fentanyl, a selective mu opioid receptor agonist, administered intravenously, influences growth hormone secretion in conscious male rats. A dose-response study demonstrated that the maximum growth hormone release was obtained with 10 micrograms/kg while higher doses were less or not effective. MR-2266 (6 mg/kg i.v.), a mu and kappa opioid receptor antagonist, and bremazocine (0.1 mg/kg i.v.) a mu opioid receptor antagonist with kappa agonistic properties, both potently inhibited the growth hormone response to fentanyl (10 micrograms/kg i.v.). In contrast, the effect of fentanyl on growth hormone release was not blocked in rats treated with either ICI-154129 (30 mg/kg i.v. or 150 micrograms/kg intracerebroventricularly a selective delta opioid receptor antagonist, or U-50488 (10 mg/kg i.v.), a specific kappa opioid receptor agonist. These results suggest that opioid receptors of the mu type are involved in the fentanyl-induced growth hormone release.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1988

The effect of bombesin on basal, alpha-methyl-p-tyrosine, haloperidol, morphine, bremazocine and stress-induced prolactin secretion.

Intravenously administered bombesin lowered basal PRL levels in conscious male rats and prevented the morphine, bremazocine and stress-induced PRL secretion. The same dose of bombesin had no effect on PRL levels in alpha-methyl-p-tyrosine pretreated rats and did not affect haloperidol-stimulated PRL release. These results show that bombesin given intravenously acts as an inhibitor of PRL secretion and suggests that it does not act on the lactotrope itself but rather by an increase of the inhibitory dopaminergic tone.

Analgesics↗
PubMed1988

The effect of beta-endorphin on basal and TRH-stimulated TSH release in conscious male rats.

The inhibitory effect of beta-endorphin (EP) or other opioids on TSH secretion is, in contrast to their stimulating properties on PRL release, still a matter of debate. In the present study a dose of 1 microgram beta-EP injected intracerebroventricularly (IVT) in unstressed conscious male rats, though highly effective on PRL release, did not affect basal TSH levels, nor the TRH-induced TSH secretion. The previously reported inhibition of TSH release by opioids may therefore be an effect only seen when pharmacological doses are used.

Animals↗
PubMed1987

In vivo and in vitro effect of naloxone on prolactin response to TRH in rat.

In adult male Wistar rats submitted to a standardized noise stress, intravenous TRH induced a prolactin (PRL) secretory response. Prior IV naloxone administration not only lowered plasma PRL levels in those stressed rats but abolished also the stimulatory action of TRH. This effect was further studied by superfusion experiments on enriched PRL cell suspensions (70% lactotrophs) from female adult Wistar rats. Naloxone kept unaffected the basal PRL secretion but lowered significantly that induced by TRH. These experiments suggest a dual effect of naloxone on rat PRL secretion, one exerted on central opioid receptors lowering stress-related increased basal PRL levels, the other inhibiting the TRH-dependent PRL secretion exerted at the lactotroph level itself.

Animals↗
PubMed1987

Opioid modulation of thyrotropin releasing hormone induced prolactin secretion.

It is known that opioids stimulate prolactin (PRL) secretion by an action on hypothalamic neurons, but in vitro studies have suggested a direct action on the lactotrophs. The present study was performed on male rats known to have little or no PRL response to TRH. A beta-endorphin (beta EP) injection in the third ventricle stimulated PRL secretion and induced furthermore a PRL secretory reaction to TRH injected intravenously 20 min later. Pretreatment with naloxone 10 min before beta EP injection abolished not only the PRL response to beta EP but also the conjugated effect of beta EP and TRH. Pretreatment with naloxone methyl bromide (Br-naloxone), a quaternary naloxone derivative, which does not cross the blood-brain barrier, had no effect on the PRL response to beta EP but prevented the conjugated effect of beta EP and TRH on PRL secretion. Pretreatment of the animals with -methyl-parathyrosine resulting in a dopamine depletion or with haloperidol, a dopamine antagonist, could not induce lactotroph responsiveness to TRH. These results suggest that beta EP in male rat sensitizes the PRL cell to TRH by a direct effect and not through an inhibition of the dopaminergic tone.

Animals↗
PubMed1987

Linear Percoll gradient centrifugation of rat anterior pituitary cells. A simple method for prolactin cell enrichment.

Prolactin (PRL) cells were purified from nulliparous normal female adult Wistar rat pituitary cell suspensions by linear Percoll density gradient centrifugation, a procedure yielding single cells. Lactotrophs were found in two different layers, the first containing 70% PRL cells in the density range 1.055 to 1.065 g/ml, the second with 28% PRL cells in the range 1.070 to 1.080 g/ml. Both cell fractions contained more than 90% viable cells with an intact ultrastructure. The physiological integrity of the 70% enriched PRL cells was assessed by their basal PRL secretion, their secretory response to TRH and dopamine, and their cAMP production in a basal situation and after incubation with dopamine.

Animals↗
PubMed1978

Specificity of action of neuraminidase, according to its bacteriological origin.

Neuraminidase from Vibrio Cholerae selectively cleaves sialic acid from FSH, but leaves the LH sialic acid, not influencing the biological activity of the latter hormone. On the other hand, Neuraminidase from Clostridium perfringens does not possess this specific action and destroys the biological activity of LH as is suggested by Parlow's OAAD-test.

Clostridium perfringens↗
PubMed1975

Selective chemical changes of gonadotropic hormones by means of neuraminidase from Vibrio cholerae.

Experiments indicate that Neuraminidase from Vibrio Cholerae selectively cleaves sialic acid derivate from FSH, but leaves the LH sialic acid derivative. By performing a specific test for LH - the OAAD test - we found that the LH activity is not influenced by the presence of Neuraminidase. The FSH activity is destroyed by Neuraminidase but the enzyme itself influences the ovarian weight, resulting in a weight decrease observed 48 hours after injection. Before or after this "critical time" no decrease is observed.

Animals↗