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Biomedical subjects

A Polleri

Publications and source records attributed to A Polleri.

At least 37 records · Page 2Linked to original sources
PubMed1987

Thyroid-stimulating hormone and prolactin responses to thyrotropin-releasing hormone in common migraine.

Intravenous administration of 50 micrograms or 200 micrograms thyrotropin-releasing hormone (TRH) to men with common migraine elicited blunted prolactin (PRL) responses, when compared with healthy controls. The thyroid-stimulating hormone (TSH) response was enhanced after 50 micrograms TRH in the migraineurs, but not after 200 micrograms. The physiologic TSH dose-response relationship was abolished in migraine sufferers. The data may be interpreted in the light of dopaminergic and noradrenergic supersensitivity, for PRL and TSH, respectively. The TSH response in migraine differs from the one that occurs in depression.

Adult↗
PubMed1986

Changes in the dopaminergic control of prolactin secretion and in ovarian steroids in migraine.

Prolactin (PRL) responses to dopamine (DA) blockers and to direct and indirect DA agonists have been studied in 23 healthy women, 17 women with catamenial migraine and 17 with non-catamenial migraine in both their follicular and luteal phases. PRL responses to the DA blockers were greater in the follicular phase of both migraine groups than in controls. The inhibitory effect of nomifensine on PRL secretion was dampened in the follicular phase of both migraine groups. These findings demonstrate an increased PRL reserve in migraine and suggest the existence of a dopaminergic supersensitivity of the lactotrophic postsynaptic DA receptors. The impaired inhibitory effect of nomifensine on PRL secretion hints at a decrease of the presynaptic DA content in tuberoinfundibular DA neurons. In migrainous women 17-beta-oestradiol levels are higher in both ovarian phases, whereas progesterone concentrations and the progesterone to oestradiol ratio are lower than in healthy subjects in the luteal phase. These data suggest the existence of a change in the oestrogen-dependent modulation of pituitary DA receptors.

Adult↗
PubMed1985

Benserazide effects on growth hormone, prolactin, and thyrotropin in normal and acromegalic man.

The effect of benserazide administration on the secretion of GH, PRL, and TSH has been considered as an index of dopamine regulatory actions. Nine acromegalic patients and nine normal subjects were given a single 125 mg oral dose of benserazide, and serum GH, PRL, and TSH were determined by RIA methods every 30 min for 4 h. Benserazide did not alter GH values either in normal subjects or in acromegalic patients. A significant increase of serum PRL was found in both groups, and the increase was similar in normoprolactinemic and in hyperprolactinemic acromegalic patients. A significant increase in TSH levels was found only in acromegalic patients. Thus, a decrease in dopamine outside the blood-brain barrier did not affect GH secretion, whereas PRL secretion was changed in the acromegalic as well as in the control group.

Acromegaly↗
PubMed1983

Neuroendocrinological signs of central neurotransmission disorders.

Modulation mechanisms of nociception have several neurotransmission interactions that are impaired in the disorder of painful perceptions. Neurotransmission changes may show up in several ways on the clinical level. They also have endocrinological correlations, since the neurotransmission systems implicated in the nociception disorders share transmitters with the regulation system operating at the pituitary level. In this sense, nocipathies exhibit analogies and may be compared to disorders of motricity and behaviour that also show endocrine changes that may be likewise explained. Though specifically different in each instance, the neurotransmission alteration that is a common denominator of these disorders allows comparisons, especially in those situations, such as the nocipathic and behavioural ones, where correlations are relevant on clinical and interpretative grounds.

Aging↗
PubMed1983

Effects of a single oral dose of phenobarbital on prolactin, growth hormone and luteinizing hormone in normal women.

The effects of a single oral dose of phenobarbital (PB) on the 24 h secretion of prolactin, growth hormone and luteinizing hormone have been evaluated in normal women. An EEG record was taken and barbiturate levels assayed in serum. A statistically significant decrease of growth hormone 24 h mean levels was observed and growth hormone and prolactin values during sleep were diminished. No changes in luteinizing hormone concentrations were observed. After PB the EEG showed no important alterations in sleep pattern, but on the power analysis an increase above 16 Hz absolute power was detected during the waking period.

Administration, Oral↗
PubMed1982

Neuroendocrinological and clinical data upon trazodone treatment in depressed patients.

Prolactin and somatotropin secretory rhythmicity was studied in 7 inhibited depression male patients, evaluated by the Hamilton Rating Scale for depression, before and after trazodone (400 mg i.v. once daily) treatment. The mean 24-hour hormone levels of the patients were comparable to the controls. Trazodone enhances the prolactin value, increasing chiefly the titres during sleep which were lower in respect to controls before treatment. The drug decreases the mean 24-hour somatotropin levels, mainly the values during sleep. A serotoninergic effect is possibly involved. An improvement of mood has been observed in all cases.

Adult↗
PubMed1980

Spontaneous nocturnal plasma prolactin and growth hormone secretion in patients with Parkinson's disease and Huntington's chorea.

Plasma prolactin (PRL) and growth hormone (GH) levels were measured in 8 patients with Parkinson's disease (PD) and in 6 patients with Huntington's chorea (HC) during the night. The sleep was evaluated with all-night poligraphic recordings. Plasma PRL levels were significantly lower in parkinsonian patients than in age-matched controls. Plasma GH values did not differ between the two groups. In HC patients no statistically significant differences were found in the PRL and GH secretory patterns when compared to the age-matched control subjects. These data indicate that changes of nocturnal PRL and GH profile in PD and HC patients in respect to age-matched healthy subjects, may be present, but a straight forward differentiation among groups is not possible because of the wide individual variations.

Aged↗
PubMed1980

Dose and sex related effects of aromatic aminoacids decarboxylase inhibitors on serum prolactin in humans.

Single doses of carbidopa and benserazide, two inhibitors of aromatic aminoacids decarboxylase, have been given orally to healthy women and men aged 19 to 32 years. Serum prolactin levels increased in respect to baseline levels when 80, 125 or 250 mg of carbidopa and 10, 20, 30, 50, 80 or 125 mg of benserazide were given. The carbidopa doses of 20 and 50 mg were ineffective. Carbidopa induced the enhancement of serum prolactin at a later time and over a longer time span than benserazide. The effect on serum prolactin is dose dependent for both drugs. The hyperprolactinaemia obtained with 250 mg of carbidopa and with 125 mg of benserazide is significantly larger in women than in age matched men. The observed prolactin increase fits with the hypothesis that a diminution of the inhibitory effect of dopamine at the pituitary and/or at the median eminence levels may occur in connection to the pharmacologically impaired monoamine synthesis. An effect of serotonin cannot, however, be excluded.

Administration, Oral↗
PubMed1979

Effects of the inhibition of aromatic aminoacids decarboxylase on prolactin secretion in humans.

Carbidopa, at the dose of 250 mg. and benserazide at the dose of 125 mg, given orally in a single dose to healthy women aged between 23 - 26 years enhance significantly serum prolactin. The effect is not shared by two other inhibitors of AADC, namely alpha-methyl DOPA (500 mg) and fentiazac (400 mg). The effect of benserazide is suppressed by bromocriptine (2.5 mg) and blunted by 1-DOPA (400 mg) given orally simultaneusly.

Adult↗
PubMed1979

Dose and sex related effects of benserazide on prolactin secretion.

Benserazide, given orally at various doses ranging from 10 to 125 mg. to healthy women aged 21 to 33 years induces a dose related increase of prolactin titres in serum. When 125 mg are administered the percent increase of the hormone is larger in women than in men.

Adult↗
PubMed1979

Lack of counteracting effect of liposomes on benserazide-induced hyperprolactinemia.

Benserazide induces an increase of serum prolactin in man, possibly as the result of an impairment of the dopamine effect on the pituitary and/or on the outer median eminence caused by the inhibition on L-dopa decarboxylase. On the other hand, liposomes obtained from bovine brain cortex phospholipids reduced serum prolactin possibly through an effect of phosphatidylserine on dopamine biosynthesis at the level of tyrosine hydroxylase. Benserazide, given orally (125 mg) to 5 normal subjects, induced an increase of serum prolactin that did not change when 300 mg of phospholipid liposomes were given intravenously 60 min later. An increase of L-dopa synthesis does not seen to be capable to overcome the effects of the decarboxylase inhibition.

Adult↗