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Biomedical subjects

A Novelli

Publications and source records attributed to A Novelli.

At least 127 records · Page 7Linked to original sources
PubMed1985

Evaluation of hypothalamic dopaminergic function by neuropharmacologic means in aged women.

The function of the hypothalamic tuberoinfundibular dopaminergic (TIDA) neurons involved in the control of prolactin secretion was investigated in aged subjects with the use of nomifensine, an indirect-acting dopamine (DA) agonist, domperidone, a DA receptor antagonist, and DA, which acts directly on the pituitary lactotropes. In all 33 women, aged 69-92 yr, were studied. Baseline prolactin values were slightly but significantly higher in aged women (13 +/- 1.2 ng/ml, M +/- S.E.M.) than in a group of control fertile women (8 +/- 0.7 ng/ml). Oral administration of nomifensine (200 mg), in 14 aged women suppressed plasma prolactin (greater than or equal to 30% of baseline) in 8 subjects, a proportion not different from that present in fertile women (7/15) also receiving a single oral dose of nomifensine. Intravenous infusion of DA (0.04 microgram/kg min, 120 min) induced a similar inhibition in plasma prolactin in the aged and the fertile women, while administration of domperidone (4 mg i.v.) evoked a higher plasma prolactin rise, 15 min post-administration, in fertile than aged women. In all, presence of baseline prolactin levels only slightly elevated and prolactin responsiveness to nomifensine and DA not different from that of fertile women denote preservation of TIDA neuronal function in old women. The blunted response to domperidone of the old women is likely attibutable to a reduced pituitary pool of prolactin.

Adolescent↗
PubMed1985

Prolactin and thyrotropin response to blockade of dopamine synthesis by monoiodotyrosine in subjects with postpartum and pathological hyperprolactinemia.

To better understand the state of dopamine (DA) neurotransmission in the tuberoinfundibular DA system (TIDA), monoiodotyrosine (3-iodo-L-tyrosine, MIT), a potent inhibitor of DA synthesis, was acutely administered to 8 normal women, 7 postpartum women, 8 women with pathological hyperprolactinemia and 5 women after successful removal of a prolactinoma. The effects on plasma prolactin (PRL) and thyrotropin (TSH) were compared to those induced in the same subjects by the DA receptor antagonist domperidone (DOM). MIT (1 gpo) and DOM (10 mg iv) induced qualitatively similar hormonal responses, although the PRL- and TSH-releasing effects of DOM were always greater than those of MIT. In control subjects, MIT treatment induced a consistent rise in plasma PRL (peak increment 45.2 +/- 13 ng/ml at 120 min); in the same subjects DOM induced a prompter and higher PRL response, (peak increment 147.8 +/- 26 ng/ml at 30 min). MIT failed to alter plasma TSH levels, while DOM induced a significant rise in plasma TSH. In postpartum women MIT induced a prompter and higher PRL rise than that occurring in controls (peak increment 180.3 +/- 20 ng/ml at 90 min), though also in this instance DOM proved to be a more potent PRL releaser (peak increment 345.7 +/- 88 ng/ml at 30 min) than MIT. MIT was unable to stimulate TSH secretion, while DOM induced a significant rise in plasma TSH. In women with pathological hyperprolactinemia MIT failed to alter baseline PRL levels while DOM slightly increased them (peak increment 14.7 +/- 3 ng/ml at 30 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1985

Comparative in vitro evaluation of the antimicrobial activity of flurithromycin by means of the MS-2 Abbott Research System.

The study reports the results of an in vitro comparative evaluation of flurithromycin by means of MS-2 research system analyzing the growth curve patterns of recently isolated strains of S. aureus, S. epidermidis, S. faecalis and H. influenzae. Flurithromycin is provided with superior activity to that of josamycin and practically superimposed on that of erythromycin. Of the 4 bacterial species studied, S. faecalis is the most sensitive, followed by Staphylococci and H. influenzae in decreasing order of sensitivity.

Enterococcus faecalis↗
PubMed1984

Hypothalamic neurotransmitter function in experimentally induced hyperprolactinemia.

It is known that animals or patients bearing a prolactin (PRL)-secreting tumor (PST) do not suppress PRL levels after administration of indirectly acting dopamine agonists, namely nomifensine (Nom), and are not responsive to the PRL releasing effect of antidopaminergic drugs and opioid peptides. Since the action of these drugs is mediated through the tuberoinfundibular dopaminergic (TIDA) system, these findings have been taken to indicate that animals and humans bearing prolactinomas have a defective TIDA function. Alternatively, PRL unresponsiveness to these drugs could be due to hyperfunction of TIDA system for the feedback action of high PRL levels. To clarify whether hypo- or hyperfunction of the TIDA system was responsible for such behaviour, we tested the effect of a synthetic opioid peptide (FK 33-824), a DA receptor antagonist, domperidone (Dom), and of Nom on PRL secretion in two experimental models of non-tumoral hyperprolactinemia, i.e. rats bearing ectopic pituitaries since 3 days (TP rats), or treated with ovine PRL (oPRL 250 micrograms, twice daily for 3 days), in which existence of an increased TIDA function has been demonstrated. FK 33-824 (0.5 mg/kg i.p.) increased significantly plasma PRL levels in control rats but failed to do so in TP rats and it elicited a significantly lower PRL response than in controls in rats treated with oPRL. In both experimental models, a PRL secretagogue, e.g. 5-hydroxytryptophan (50 mg/kg i.p.), elicited the same response as in controls, indicating that the pituitary PRL pool was preserved.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

In vivo supersensitivity of the anterior pituitary of old female rats to dopaminergic inhibition of prolactin secretion.

Old female rats (20-27 months) were given acute administration of an indirectly acting dopamine (DA) agonist, nomifensine or scalar doses of the direct DA receptor agonist, bromocriptine. Young female rats (4-9 months) were used as controls. Nomifensine (10 mg/kg i.p.) decreased significantly basal prolactin (PRL) levels in young rats as in old rats. In young rats, bromocriptine decreased significantly basal PRL levels only at the dose of 0.5 mg/kg intraperitoneally, the doses of 0.1 and 0.02 mg/kg being ineffective. In contrast, in old rats administration of 0.02 mg/kg of bromocriptine consistently inhibited basal PRL levels and the maximum PRL-lowering effect was already evident at the dose of 0.1 mg/kg. These data indicate that the pituitary of old rats, due to the age-related removal of dopaminergic inputs from the tuberoinfundibular system, becomes supersensitive to direct dopaminergic stimulation. This phenomenon may explain the normal PRL responsiveness of old rats to nomifensine, despite defective tuberoinfundibular dopaminergic function.

Adenoma↗
PubMed1984

Dynamic testing of prolactin and growth hormone secretion in patients with neuroendocrine disorders.

Prolactin (Prl) and growth hormone (GH) responses to different pharmacologic probes acting at the central nervous system (CNS) or the anterior pituitary (AP) level were evaluated in patients with distinct neuro-endocrine disorders. Thirteen patients with Prl-secreting tumours (PST), 10 acromegalics (A) and 8 patients with hypothalamic lesions (HL), as assessed on clinical, radiological and surgical grounds, underwent on separate occasions acute testing with the opioid peptide FK 33-824 (0.5 mg iv), the indirect dopamine (DA) agonist nomifensine (NOM, 200 mg po), the DA receptor antagonist domperidone (DOM, 10 mg iv), TRH (200 microgram iv) and insulin (ITT, 0.10-0.15 IU/kg iv). All patients were evaluated pre-surgery and 4 of them also post-surgery. Prl and GH were evaluated by RIA at different time intervals following treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1984

Clinical chemotherapeutic evaluation of fosfomycin plus amoxicillin (co-fosfolactamine): a prospective double-blind clinical trial.

Seventy-three hospitalized patients with urinary tract infections (UTI) were included in a double-blind study and received at random either fosfomycin or fosfomycin plus amoxicillin (CFL) in a pre-fixed combination, in order to evaluate the effectiveness of the CFL. CFL was administered orally to 39 patients at the daily dosage of 1 g every 8 h for 6 days (666 mg of fosfomycin and 334 mg of amoxicillin) while fosfomycin was given orally to 34 patients at the daily dosage of 666 mg every 8 h for 6 days. A bacteriological cure was observed in 97.4% of the patients treated with CFL, while in the fosfomycin group the bacterial eradication was obtained only in 82.3% (P less than 0.05). CFL showed a more rapid bactericidal activity than fosfomycin. In addition, CFL was more effective than fosfomycin against "difficult" Gram-negative bacteria such as Proteus spp. and Pseudomonas aeruginosa. Both antibiotics were well tolerated. Our limited experience revealed that CFL induces a negligible degree of resistant strains, and fewer than fosfomycin. Thus we conclude that CFL seems to be a useful antibiotic combination in the treatment of UTI.

Adult↗
PubMed1984

Bacillus subtilis spores as a natural pro-host oral agent. Preliminary data in children.

The commercial preparation of Bacillus subtilis spores may be considered within the classification of biological response modifiers (BRM's) and included among exogenous natural substances. Recently we decided to study the effect of a long-term B. subtilis spores oral treatment in children suffering from recurrent infectious diseases of the respiratory tract. Fifty-three children 5-9 years old have been studied. The clinical valuative parameter was the number of days of absence from school during a 4-month period. In another group of 12 diseased children, mean age 5.5 yrs we recently initiated a laboratory immunological evaluation of peripheral lymphomonocytes in relation to an oral treatment with B. subtilis spores for at least 2 months. Our results show that B. subtilis spore therapy significantly reduced the frequency of respiratory tract infections in the group of treated children. In addition, preliminary immunological laboratory evaluation demonstrated a complete return to the normal lymphomonocyte status after at least 2 months of treatment with B. subtilis spores.

Adjuvants, Immunologic↗
PubMed1983

Neuroendocrine studies with fluvoxamine: animal data.

1 Administration of the potent 5-hydroxytryptamine (5-HT) re-uptake inhibitor fluvoxamine (25 mg/kg i.p. for 14 days) to adult cycling female rats did not alter either the number of oestrous episodes or the plasma concentrations of luteinizing hormone determined on days 2, 9 and 14 of treatment. 2 Fluvoxamine (25 mg/kg i.p.) induced in male rats a clear-cut lowering of beta-endorphin-like immunoreactivity from the anterior pituitary, but not the neurointermediate lobe, and increased concomitantly plasma levels of beta-endorphin and beta-lipotropin. 3 Fluvoxamine (12.5 and 25 mg/kg i.p.) stimulated, although not strikingly, prolactin (PRL) secretion in adult male rats, and at 25 mg/kg i.p. potentiated the PRL-releasing effect of 5-hydroxytryptophan (30 mg/kg i.p.). 4 In male rats treated daily with fluvoxamine (25 mg/kg i.p.) the PRL-releasing effect of an additional acute fluvoxamine administration (same dose) was abolished after 4 days maintenance treatment. One week after withdrawal of maintenance, which had been given for 14 days, the challenge dose of fluvoxamine was still unable to raise plasma PRL levels. 5 The endocrine effects of acute fluvoxamine administration are compatible with activation of 5-HT neurotransmission in the central nervous system. The mechanism(s) underlying tolerance to the PRL-releasing action of the drug is presently obscure. Its elucidation should provide insight into the mechanism of action of antidepressant drugs affecting 5-HT function.

5-Hydroxytryptophan↗
PubMed1983

Prolactin-lowering and -releasing drugs. Mechanisms of action and therapeutic applications.

Drugs whose systemic and/or central administration induce suppression or stimulation of prolactin secretion are reviewed. The most commonly used prolactin-lowering drugs include: (a) direct-acting dopamine receptor agonists (e.g. dopamine, apomorphine and the ergot derivatives); (b) indirect-acting dopamine agonists (e.g. amphetamine, nomifensine, methylphenidate, amineptine); (c) drugs which impair serotoninergic neurotransmission (e.g. the neurotoxin 5,7-dihydroxytryptamine and the serotonin receptor antagonists methysergide and metergoline); (d) gamma-aminobutyric acid [GABA]-mimetic drugs (e.g. GABA, muscimol, ethanolamine-O-sulphate, sodium valproate); (e) histamine H2-receptor agonists; and (f) cholinergic (muscarinic and nicotinic) receptor agonists. Major prolactin-stimulating agents comprise: (a) dopamine receptor antagonists (e.g. classic and atypical antipsychotic drugs); (b) drugs differently capable of impairing central nervous system dopamine function (e.g. blockers of dopamine neurotransmission such as alpha-methyl-p-tyrosine and 3-iodo-L-tyrosine, false precursors such as alpha-methyldopa, and inhibitors of L-aromatic amino acid decarboxylase such as carbidopa and benserazide); (c) drugs enhancing serotoninergic neurotransmission (e.g. the serotoninergic precursors tryptophan and 5-hydroxytryptophan, direct-acting serotonin agonists such as quipazine and MK 212, and indirect-acting serotonin agonists such as fenfluramine); (d) blockers of serotonin reuptake (e.g. fluoxetine, fluvoxamine and clovoxamine); (e) H1-receptor agonists; and (f) H2-receptor antagonists (e.g. cimetidine). Some of the above classes of drugs (e.g. the indirect-acting dopamine agonists, dopamine receptor antagonists, GABA-mimetic drugs, dopamine receptor blocking drugs, and H2-antagonists) may be useful for selecting among hyperprolactinaemic patients those with a prolactin-secreting tumour in an early stage of the disease. Direct-acting dopamine receptor agonists, notably the ergot derivatives; are potent antigalactopoietic agents, can revert impaired gonadal function to normal in both female and male patients with hyperprolactinaemia, and may have antiproliferative effects on pituitary prolactin-secreting tumours. All prolactin-stimulating agents, but especially the dopamine receptor antagonists, are liable to induce alterations in gonadal function in subjects of either sex. In addition to their usage for diagnostic or therapeutic purposes, the above drugs appear to be invaluable tools for enabling a better understanding of the neurotransmitter control of prolactin secretion.

Animals↗
PubMed1982

Thyrotrophin and prolactin responses to thyrotrophin-releasing hormone in patients with Parkinson's disease.

The thyrotrophin (TSH) and prolactin (Prl)-releasing effects of TSH-releasing hormone (TRH) were investigated in 20 subjects with Parkinson's disease (PD), unmedicated, on chronic treatment with a combination levodopa-benserazide (Madopar) or levodopa-carbidopa (Sinemet) or withdrawn from therapy. Administration of TRH (200 micrograms iv) induced in unmedicated patients TSH and Prl responses significantly lower than those of sex-and age-matched controls. In patients on Madopar therapy the TSH and Prl responses to TRH were greater than in unmedicated patients and comparable to those of controls, while in patients on Sinemet therapy the pituitary responses were undistinguishable from those of unmedicated subjects. Withdrawal of Madopar therapy resulted in a marked diminution of the TSH response but did not affect the Prl response to TRH. Withdrawal of Sinemet therapy did not alter the TSH and Prl responses to TRH. Concomitant evaluation of growth hormone (GH) levels, in none of the subjects evidenced non-specific changes in plasma GH following TRH. Since TSH and Prl responses to TRH are inhibited by an enhancement of the dopaminergic tone, it would appear that the latter is preserved in the tuberoinfundibular system of unmedicated subjects and subjects on chronic Sinemet therapy, but is defective in subjects on chronic Madopar therapy.

Adult↗
PubMed1981

Growth hormone and prolactin stimulation by Madopar in Parkinson's disease.

Madopar, a combination of levodopa with benserazide, induced an inconsistent rise in plasma growth hormone in unmedicated patients with Parkinson's disease and in controls, and a greater growth hormone rise in Parkinsonian subjects on chronic Madopar therapy. In subjects on chronic therapy with levodopa and carbidopa (Sinemet), the growth hormone releasing effect of Madopar was blunted. Madopar increased plasma prolactin (PRL) in controls, unmedicated patients and patients on Madopar therapy while in patients on Sinemet therapy the PRL-releasing effect of Madopar was strikingly reduced. Since these data were interpreted as due to a defective dopamine tone in the hypothalamus of Parkinsonian subjects on Madopar but not Sinemet therapy, a direct dopamine receptor agonist, lisuride was administered. Lisuride, however, elicited a blunted growth hormone response both in patients on Madopar and Sinemet therapy, without revealing a state of supersensitivity of dopamine receptors for growth hormone control in Parkinsonian subjects on Madopar therapy. No difference was present in the PRL-lowering effect of lisuride in the different experimental groups. These findings suggest that: (1) hypothalamic dopamine function is impaired in Parkinsonian subjects on Madopar therapy, preserved in unmedicated patients and enhanced in patients on Sinemet therapy; (2) the endocrine effects observed in Parkinsonian subjects on chronic Madopar therapy may be due to some penetration of benserazide across the blood brain barrier in the region of the hypothalamus; (3) since Madopar and Sinemet are in essence equally effective antiparkinsonian remedies, penetration of benserazide does not occur across the blood brain barrier surrounding the nigrostriatal system.

Adult↗