Search PubMed⌕ Search

Biomedical subjects

F Camanni

Publications and source records attributed to F Camanni.

At least 199 records · Page 11Linked to original sources
PubMed1978

Increased thyrotrophin secretion induced by sulpiride in man.

100 mg i.m. sulpiride (a dopamine-receptor-blocking drug) led to a significant rise in plasma TSH in normal womem, in female patients with galactorrhoea, and, to a much more marked degree, in male and female patients with primary hypothyroidism. In the hypothyroid patients, there was a significant positive correlation between basal TSH and its maximum increment after sulpiride. The drug proved to be an even more potent stimulator of PRL, at least in subjects with normal blood PRL. Normal males, on the other hand, displayed no significant changes in TSH after sulpiride. Continuous administration (150 mg/day per os for 15 days) also resulted in enhancement of TSH in normal women. These results suggest that TSH release is controlled by a dopaminergic mechanism in man. The more accentuated TSH response in hypothyroid patients may perhaps be attributable to the absence of negative-feedback on the part of thyroid hormones.

Adolescent↗
PubMed1978

Effects of bromocriptine on adenylate cyclase and phosphodiesterase activities of rat striatum.

The activity of 2-bromo-alpha-ergokryptine (bromocriptine) (5 mg kg-1, i.p.) on adenylate cyclase and on phosphodiesterase (PDE-PDE II) of rat striatum, has been examined both in vitro and in vivo. In vitro and in vivo bromocriptine stimulated adenylate cyclase activity, but reduced the stimulating effect of dopamine on adenylate cyclase activity. Bromocriptine showed a dose-dependent biphasic action on phosphodiesterases in vitro while in vivo it stimulated them. The results obtained proved bromocriptine to have an agonist-antagonist action at striatal dopamine receptor level, with a relevant effect on the cAMP system.

Adenylyl Cyclases↗
PubMed1978

Carbidopa inhibits the growth hormone- and prolactin-suppressive effect of L-dopa in acromegalic patients.

The plasma GH, PRL, TSH, and dopamine (DA) responses to an infusion of L-dopa were examined in six acromegalic patients before and after pretreatment with carbidopa, a drug which inhibits the peripheral conversion of L-dopa to DA. Carbidopa neither modified baseline DA nor induced changes in baseline GH, PRL, or TSH levels. The drug instead markedly reduced the L-dopa-induced DA rise, an effect which was concomitant to a striking reduction of the suppressive effect of L-dopa on plasma GH and a partial inhibition of the suppressive effect of L-dopa on plasma PRL. TSH levels did not change either after L-dopa alone or L-dopa plus carbidopa. These data demonstrate that in "responder" acromegalics, L-dopa inhibits GH secretion through its peripheral conversion to DA and not via activation of central DA neurotransmission. For the effect of L-dopa on PRL secretion, in addition to a peripheral dopaminergic component, a central component cannot be disregarded.

Acromegaly↗
PubMed1977

Effect of dopamine on plasma growth hormone and prolactin levels in normal and acromegalic subjects.

In contrast with other dopaminergic drugs (L-dopa, apomorphine or bromocriptine) a 280 mug/min dose of dopamine infused for 120 min failed to induce an increase in plasma GH in 9 normal subjects. During dopamine infusion, no significant change in the GH response to arginine was also noted, whereas prolactin displayed a significant fall. In 15 acromegalic patients, on the other hand, the drug caused a marked fall in both GH (mean+/-SE; 71.1%+/-5.6) and prolactin (mean+/-SE; 67.6%+/-4.0) followed by a distinct rebound after the end of the test. There was a very close relation (P less than 0.001) between the maximum per cent decrease in GH during dopamine and after 2.5 mg bromocriptine by mouth. Dopamine also inhibited the GH response to TRH (4 patients). Since dopamine does not readily cross the blood-brain barrier, these results suggest that the stimulating effect of dopaminergic drugs on GH secretion in the normal subject is exerted via the CNS, whereas in acromegaly there is a direct action on structures lying outside the blood-brain barrier, probably in the hypophysis. Dopaminergic inhibition of prolactin is primarily the result of action on the hypophysis, as well as on the hypothalamus, in both normal and acromegalic subjects.

Acromegaly↗
PubMed1977

Long-term treatment with 2-Br-alpha-ergocryptine in acromegaly.

Thirty acromegalic subjects underwent chronic CB154 therapy (10-20 mg daily) for periods ranging from 3 months up to 2 years. In 18 out of 21 patients, who exhibited consistent HGH reduction following acute administration of the drug, there was also during chronic treatment, a suppression of the plasma HGH levels exceeding 50% of base line values, e.g. from mean daily values between 14-197 ng/ml (mean +/- SEM = 57.8 +/- 12.4 ng/ml pre-treatment) to 2-19 ng/ml (mean 8.3 +/- 1.2 ng/ml post-treatment). In 12 of the subjects who responsed to chronic CB154 treatment, the mean daily values of HGH were below 10 ng/ml. The suppression of plasma HGH was maintained unaltered throughout the whole course of therapy. In the 9 subjects, in whom no consistent HGH decrease was evidenced with acute CB154 administration, there was accordingly a minor or no suppression of HGH values during the chronic treatment. In 13 subjects, irrespective of the degree of their GH responses, the plasma prolactin levels were constantly inhibited by CB154; instead the drug failed to modify significantly the TRH or insulin-induced GH release. These changes in the hormonal parameters were paralleled by marked clinical amelioration and improvement of some of the metabolic alterations frequently encountered in acromegaly, e.g. reduced carbohydrate tolerance, increased insulin resistance, diminished fall of plasma phosphorus after insulin, decreased urinary excretion of phosphate, hyper-hydroxyprolinuria and hyper-calciuria. Collectively, these data demonstrate that CB154 thrapy is effective in reducing HGH hyper-secretion in many acromegalic patients during long-term treatment.

Acromegaly↗
PubMed1975

[Effects of propranolol on some metabolic changes induced with insulin].

The effect of propranolol on certain insulin-induced metabolic changes in man. The effects of 0.2 mg/kg/body weight propranolol perfused in 10' on insulin-induced (0.15 I.U./Kg i.v.)changes in blood glucose, pyruvate, lactic acid, phosphorus, and potassium levels were examined in 12 normal volunteers. The blood glucose curve was substantially unaffected. Insulin-induced increases in lactate and pyruvate were inhibited to a varying degree, namely 78% (61-93%) and 44% (0.94%) respectively. The fall in phosphorus was reduced in a more constant manner (mean 48; range 37-57%) in all subjects, while that of potassium was not altered. The data indicate that these insulin-induced changes are significantly, though variably, attributable to beta-adrenergic activity on the part of endogenous catecholamines released during insulin-induced hypoglycaemia.

Blood Glucose↗
PubMed1975

Effect of five dopaminergic drugs on plasma growth hormone levels in acromegalic subjects.

The effect of 5 dopaminergic drugs, 2-Br-alpha-ergocryptine (CB 154), L-dopa, 1-(2-pyrimidyl)-4-piperonylpiperazine (Piribedil), amantadine and 1,3-dimethyl-5-amino-adamantan (d 145), on human growth hormone levels (hGH) was studied in 38 acromegalic subjects. Acute administration of CB 154 (2.5 mg p.o.) in 34 patients was followed by a significant and sustained fall in plasma hGH levels; in 19 cases (55.6%) the observed fall was clearly below the +/- 2SD of the mean GH changes present in the same subjects after placebo. In patients previously shown to be responsive to CB 154, Significant GH falls were also present following the single administration of L-dopa (500 mg p.o.) (9 patients) and Piribedil (100 mg p.o.) (5 patients), although CB 154 exhibited a more frequent, striking (reduction of up to 1-2 ng/ml) and long-lasting (4 h more) effect. In contrast, amantadine (200 mg p.o.) or D 145 (20 or 50 mg p.o.) did not induce significant changes in hGH levels (7 patients). These results broaden and corroborate previous findings on the hGH-lowering effect of dopaminergic stimulation in acromegaly. The possible reason(s) for the difference in hGH response with different dopaminergic compounds is discussed.

Acromegaly↗
PubMed1975

Changes in plasma growth hormone levels in normal and acromegalic subjects following administration of 2-bromo-alpha-ergocryptine.

2-Bromo-alpha-ergocryptine (CB-154), AN ERGOT ALKALOID THAT STIMulates dopaminergic receptors, caused a widely varying, but significant increase in plasma GH levels in normal subject whereas a marked and protractedfall in values was observed in some patients with acromegaly. It is suggested that these effects were mediated by activation of either hypothalamic or hypophyseal dopaminergic receptors. The fact that GH values fell to or near normal levels in 4/8 cases suggests that CB-154 may have therapeutic possibilities in acromegaly.

Acromegaly↗