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Biomedical subjects

F Massara

Publications and source records attributed to F Massara.

At least 37 records · Page 2Linked to original sources
PubMed1983

Glucagon-induced increase in plasma potassium levels in type 1 (insulin-dependent) diabetic subjects.

To investigate the hypothesis that in Type 1 (insulin-dependent) diabetes the increase in plasma potassium during decompensation may be due to a rise in glucagon concentrations, we have measured plasma glucose, potassium and glucagon levels in five diabetic patients during two tests with 0.154 mol/l saline or somatostatin (500 micrograms/h) performed on two successive days. The patients were maintained normoglycaemic overnight by means of a continuous insulin infusion. After insulin withdrawal during the saline infusion, glucose and potassium levels rose markedly (delta maximum: glucose, 12.0 +/- 1.5 mmol/l; potassium, 0.73 +/- 0.12 mmol/l), while glucagon showed a slight, but significant increment (delta maximum: 10.6 +/- 1.0 pmol/ml, p less than 0.05). The potassium increment was not mediated by a reduction in blood pH. Somatostatin abolished the rise in glucagon concentration and simultaneously markedly inhibited the rise in potassium and glucose levels. It is concluded that in acute insulin deficiency, glucagon could be one of the factors that contributes to hyperkalaemia.

Adolescent↗
PubMed1983

Reciprocal pattern of the TSH and PRL responses to dopamine receptor blockade in women with physiological or pathological hyperprolactinaemia.

The TSH and PRL responses to administration of the two dopamine (DA) receptor antagonists sulpiride and domperidone, were studied in fifteen normoprolactinaemic subjects, twenty-two post-partum women and sixteen subjects with presumptive evidence of (six subjects) or surgically confirmed (ten subjects) prolactinomas. Sulpiride (100 mg i.m.) or domperidone (10 mg i.v.) elicited a slight increase in basal TSH levels in both normoprolactinaemic and post-partum women, but induced a clear-cut TSH rise in subjects with a tumour. Conversely, sulpiride and domperidone strikingly stimulated PRL secretion in normoprolactinaemic and post-partum women, but only slightly enhanced base-line PRL levels in women with prolactinomas. The reason for the reciprocal pattern of TSH and PRL responsiveness to DA receptor blockade of post-partum women and subjects with prolactinomas is presently obscure. Since baseline PRL levels in the two hyperprolactinaemic states overlapped widely, it would appear that hyperprolactinaemia per se is not responsible for such behaviour.

Adolescent↗
PubMed1983

Defective regulation of prolactin secretion after successful removal of prolactinomas.

The PRL response to nomifensine (Nom), an indirect DA agonist; domperidone (Dom), a DA receptor antagonist; and TRH, which directly stimulates the PRL-secreting cells, was evaluated 2-53 months after surgery in 13 patients in whom successful removal of a prolactinoma had resulted in normal serum PRL levels and return of regular menses or libido and potency. In addition, the pattern of TSH secretion in response to Dom and the spontaneous rise in plasma PRL of 6 cured patients during pregnancy were evaluated. Nom induced an inconsistent decrease in basal PRL levels, a pattern contrasting with that in healthy women in whom plasma PRL was markedly suppressed after administration of the drug. Dom and TRH elicited a significant rise of basal PRL levels, but the rise was markedly lower than that occurring in the control group. The TSH increment after Dom treatment was lower than that before surgery, though higher than that in the controls. Evaluation of individual patients showed that only one patient had a normal PRL response to either Nom or Dom, while the TSH response to the latter returned to normal in five of seven patients. During pregnancy, plasma PRL rose inconsistently in the patients, and PRL levels were generally lower than those in normal pregnant women. These results suggest the presence of an abnormality in the dopaminergic mechanism(s) of PRL control before and after adenomectomy or, less likely, the existence of impaired pituitary function or reserve.

Adenoma↗
PubMed1983

Effects of naloxone on the insulin and GH responses to alpha-adrenergic stimulation with clonidine.

To find if endorphins can influence hormonal responses mediated by noradrenergic pathways, we examined the effects of naloxone, an opiate receptor blocker, on the GH and insulin responses to clonidine, a drug which acts by stimulation of alpha-adrenergic receptors. Intravenous clonidine (0.15 mg in 10 min) induced a significant fall of plasma insulin and a marked increase of plasma GH. Intravenous naloxone (bolus of 1.6 mg followed by 50 micrograms/min) did not change the insulin response to clonidine, and seemed to induce only a slight delay in the GH response.

Adrenergic alpha-Agonists↗
PubMed1982

Impaired prolactin responsiveness to dopamine antagonists in acromegaly.

Prolactin (PRL) and growth hormone (GH) secretion have been evaluated in 17 acromegalic patients following acute administration of two dopamine (DA) receptor antagonists, i.e. sulpiride (SULP) and domperidone (DOM). Six patients had persistent hyperprolactinemia. In 8 normoprolactinemic patients, i.m. injection of 100 mg SULP elicited only a slight rise iN plasma PRL, which was strikingly lower than that SULP induced in control subjects. Likewise, an i.v. bolus injection of DOM (4 mg) was barely effective to raise plasma PRL in the 11 normoprolactinemic and the 6 hyperprolactinemic patients. DOM was instead capable of inducing a clear-cut rise in plasma PRL in normoprolactinemic controls and in a group of subjects with puerperal hyperprolactinemia. Neither drug affected GH secretion in acromegalic patients. It is proposed that a defective tuberoinfundibular DA function or, alternatively, a diminished PRL reserve due to a decrease pituitary lactotroph mass may be responsible for the blunted PRL responsiveness of acromegalics. However, standing the paucity of present knowledge on the pituitary PRL secretory pool in acromegalics, neither hypothesis seems capable to account satisfactory for the reported results.

Acromegaly↗
PubMed1981

Dicentric Y chromosome in a patient with gonadal dysgenesis and seminoma.

A male patient with ambiguous external genitalia developed a seminoma in the left inguinal region; his internal genitalia included a streak gonad on the right and a small uterus. Cytogenetic studies demonstrated a dicentric Y chromosome with unstable behavior during cell division, which resulted in 45,X/46,X,dic(Y)/47,X,dic(Y),dic(Y) mosaicism. Immunogenetic studies allowed the identification of the male-determining H-Y antigen on both leukocytes and red cells of the patient. The significance of these results is discussed with respect to recent data on the genetic control of H-Y antigen.

Adult↗
PubMed1981

Tests of prolactin secretion in the diagnosis of hyperprolactinemic states: nomifensine and domperidone.

Forty-one subjects with hyperprolactinemia underwent testing on separate occasions with nomifensine, an indirectly acting dopamine agonist, and domperidone, a dopamine receptor-blocking agent. Nomifensine (200 mg orally) did not significantly modify plasma levels of prolactin (PRL) in 17 subjects in whom the existence of a pituitary tumor had been established at surgery (12 subjects) or was highly probable (5 subjects). Of the remaining 24 patients with hyperprolactinemia of uncertain etiology, 6 had PRL responsiveness to nomifensine (decrease of baseline PRL levels greater than or equal to 30%) and 18 had PRL unresponsiveness to the drug. The administration of domperidone (4-mg bolus injected intravenously) showed in 36 of the 41 patients the existence of a homogeneity between PRL responsiveness to nomifensine and PRL responsiveness to domperidone. In only five patients was failure of nomifensine to lower plasma PRL levels associated with an increase in plasma PRL levels after domperidone administration (at least doubling of baseline PRL levels). The combined application of nomifensine and domperidone tests holds promise of being a useful method for distinguishing among hyperprolactinemic subjects those with a prolactinoma.

Adenoma↗
PubMed1981

Increased thyrotrophin and prolactin secretion induced by domperidone in hypothyroid subjects.

The thyrotrophin (TSH) and prolactin (Prl) releasing effects of domperidone, a recently developed antidopaminergic drug which does not cross the blood-brain barrier, were investigated in 8 women affected by primary hypothyroidism, and were compared to those elicited by another antidopaminergic drug, sulpiride. Domperidone (4 mg iv) induced a clear-cut and sustained rise in both plasma TSH and Prl, with peak levels occurring 15 and 30 min post-injection, respectively. The increments in plasma Prl after domperidone were significantly higher than those in plasma TSH. The TSH and Prl responses induced by domperidone were almost superimposable to those provoked in the same subjects by sulpiride (100 mg im). In view of the inability of domperidone to penetrate into the central nervous system (CNS), these findings imply a 'peripheral' site(s) of action (i.e. anterior pituitary and/or median eminence) for the effect of antidopaminergic drugs on TSH secretion, and, re-iterate the notion that the same 'peripheral' sites are involved in the Prl-releasing effect of these compounds.

Adolescent↗
PubMed1981

The risk of pronounced hyperkalaemia after arginine infusion in the diabetic subject.

Following previous work showing that i.v. arginine induces a fall in blood phosphorus and an increase in blood potassium in normal subjects, investigation of the mechanism underlying these metabolic changes was extended to a group of 14 insulin-dependent diabetics and a further 6 normal volunteers. In the diabetics, arginine (0.5 g/kg body weight) in 30 min caused a slight, but significant fall in blood phosphorus (delta = -0.40 +/- 0.04 mg/ml p less than 0.01). This was well below the fall noted in the normal subjects, which, as demonstrated in the earlier study, is to a great extent mediated by insulin. The increase in blood potassium was much more marked than in the normal subjects (delta = + 1.42 +/- 0.15 mEq /l; p less than 0.001) and rose to pathological levels (5.6 to 6.5. mEg/l) in 9 out of 14 patients. There were no significant changes in blood pH, plasma osmolality, or plasma aldosterone. Inhibition of the glucagon response to arginine by means of a priming dose of 250 micrograms somatostatin, followed by infusion of 1,500 micrograms/hr, did not abolish the rise in blood potassium. These findings indicate that insulin protect against arginine-induced hyperkalaemia and that this metabolic alteration does not depend on glucagon, acidosis, enhance plasma osmolality, nor the suppression of aldosterone secretion. Persons with low insulin secretion due, for example, to stress or diabetes, run the risk of pathological hyperkalaemia if subjected to i.v. infusion of arginine.

Adolescent↗
PubMed1980

Influence of glucagon on plasma levels of potassium in man.

To investigate the role played by glucagon in the regulation of plasma potassium, we have examined the behaviour of this ion during four 2 h infusions of saline, glucagon (200 ng/min), cyclic somatostatin (priming dose of 50 microgram followed by 5.8 microgram/min) and somatostatin plus glucagon in 6 normal volunteers. Glucagon alone produced no change in potassium, despite an increase in insulin. Somatostatin, in addition to depressing insulin, produced a slight but significant (P < 0.01) increase in potassium (delta max: 0.2-0.8 mmol/1: mean +/- SEM, 0.4 +/- 0.1). Infusion of somatostatin together with glucagon suppressed the glucagon-induced increase in insulin and greatly augmented the increase in blood glucose. Potassium rose significantly more (P < 0.02) than after somatostatin alone (delta max: 0.5-1.3 mmol/l; mean 0.9 +/- 0.1), indicating that hyperkalaemia results from hyperglucagonaemia in the absence of insulin. Evidence is presented that this last phenomenon is not mediated by hyperglycaemia or by a reduction in aldosterone secretion. It is suggested that low blood insulin and increased glucagon could be one of the mechanisms that underlie or magnify the hyperkalaemia observed in cases of serious stress or decompensated diabetes.

Adult↗
PubMed1980

Hormone patterns during bromocriptine-induced pregnancy in hyperprolactinemic patients.

Plasma prolactin (PRL) and human placental lactogen (HPL), and urinary estriol and pregnanediol were studied during pregnancies induced with bromocriptine (Parlodel, Sandoz) in 10 cases of hyperprolactinemia. Previous selective adenomectomy or intrasellar implantation of radioactive gold (198Au) failed to induce a complete remission in 3 of these subjects. PRL rapidly increases after bromocriptine withdrawal, reaching values higher than those in normal women in the same stage of pregnancy within a few weeks. At term, pathological PRL levels occurred in 3 subjects only (with distinct alterations of the sella turcica). Estriol, pregnanediol and HPL were normal in all cases. These findings suggest that PRL levels higher than those normally observed during pregnancy do not alter fetoplacental endocrine function.

Adult↗
PubMed1980

Prolactin-releasing effect of domperidone in normoprolactinemic and hyperprolactinemic subjects.

The prolactin (PRL)-releasing effect of domperidone (DOM), a novel antidopaminergic drug which does not cross the blood-brain barrier, was investigated in normoprolactinemic subjects, in subjects with physiologic puerperal hyperprolactinemia or pathological hyperprolactinemia. DOM (4 mg i.v.), administered to 8 normoprolactinemic women, induced a clear-cut and sustained rise in plasma PRL, with peak levels occurring 15-30 min postinjection; the effect of the drug was also evident in 3 normoprolactinemic women at the dose of 0.25 mg i.v. Also in 8 puerperal women (postpartum day 2) intravenous administration of 4 mg DOM was followed by an increase in plasma PRL (51-517% of baseline levels, 15-45 min postinjection). Administration of DOM (4 mg i.v.) to 16 subjects with pathological hyperprolactinemia, evidenced the presence of 14 DOM-nonresponder (maximum percent increase of baseline PRL 48%) and 2 DOM-responder subjects. In 8 of the DOM-nonresponder subjects the existence of a pituitary tumor was established at surgery by selective removal of an adenoma (7 subjects) or a teratoma (1 subject): of the 6 subjects who did not undergo surgery, 3 had biochemical and/or radiologic evidence suggestive of a PRL-secreting tumor and 1 was acromegalic. These results indicate that DOM is capable of releasing PRL both in normoprolactinemic subjects and subjects with puerperal hyperprolactinemia. In contrast, DOM is unable to modify PRL levels in most subjects with pathological hyperprolactinemia, with proven or suspected pituitary tumors.

Adenoma↗
PubMed1980

Effect of sulpiride on plasma prolactin levels in women with puerperal or pathological hyperprolactinaemia.

The effect of 100 mg im sulpiride on plasma Prl levels was studied in 10 normal females, 21 patients with galactorrhoea and normal plasma Prl, 10 women with puerperal hyperprolactinaemia and 27 patients with amenorrhoea-galactorrhoea and high plasma Prl levels. The response to sulpiride in patients with galactorrhoea but normal PRL was slightly higher (P < 0.05) than that observed in normal women, but only if expressed in per cent. Women with puerperal hyperprolactinaemia respond to the drug with a marked increase in Prl (mean +/- SEM: 563.0 +/- 142.8%), even though their baseline values are already very high (mean +/- SEM: 133.6 +/- 23.8 ng/ml). By contrast, there is a lower or no response to sulpiride in 13 women with pituitary tumour. The same was true in 11 patients with hyperprolactinaemia of uncertain aetiology but also 10 of these subjects presented signs suggestive of a tumour. In the last 3 patients with pathological hyperprolactinaemia in whom a consistent Prl increase after sulpiride was observed, hyperprolactinaemia was probably not of tumourous origin. On the basis of these results, the sulpiride test appears promising for discriminating between organic and 'functional' cases of enhanced Prl secretion.

Adult↗