Search PubMed⌕ Search

Biomedical subjects

S G Cella

Publications and source records attributed to S G Cella.

79 records · Page 5Linked to original sources
PubMed1984

Growth-hormone releasing factor and clonidine in children with constitutional growth delay. Evidence for defective pituitary growth hormone reserve.

Six male prepubertal children with constitutional growth delay (CGD), and a subnormal growth hormone (GH) response to insulin hypoglycemia, and four normal prepubertal children were given in different occasions 1 microgram/Kg iv synthetic hpGRF-40 or a single oral dose of 0.15 mg/m2 clonidine (Clon), an effective growth hormone (GH) secretagogue. In the normal children brisk and clear-cut GH rises were detected in plasma after hpGRF-40 (peak GH levels at 15-30 min) or clonidine (peak GH levels 60-90 min). In CGD children hpGRF-40 induced a biphasic response, e.g. a slight increase in plasma GH at 15 min followed by a delayed and erratic GH rise occurring 45-120 min post-injection. Also the GH response to Clon was sluggish and delayed and peak plasma GH levels were attained only 90-180 min post-drug administration. These data indicate that the CGD children of our study have a defect in the pituitary GH reserve.

Child↗
PubMed1984

Inhibitory action of the alpha 1-adrenergic receptor on growth hormone secretion in the dog.

Intravenous administration of methoxamine ( METHOX , 5 mg, iv), a specific alpha 1-adrenergic agonist, reduced baseline GH levels of four unanesthetized beagle dogs 45 and 60 min post-injection and completely abolished the GH-releasing effect of the alpha 2-adrenergic agonist clonidine ( CLON , 4/ micrograms/kg, iv). Prazosin (PRA, 0.1 mg/kg, iv), an alpha 1-adrenergic antagonist, administered before METHOX re-instituted the GH-releasing effect of CLON . METHOX administered at the starting of an arginine infusion (ARG, 10% solution, 3.3 ml/min X 30 min) reduced consistently the GH releasing effect of the latter while, conversely, pretreatment with PRA, strikingly potentiated the GH-releasing effect of the amino acid (2 dogs). METHOX did not alter the GH-releasing effect of human pancreatic GH-releasing factor (hpGRF-40, 1/microgram/kg, iv), though it consistently delayed the occurrence of the GH secretory peak following hpGRF-40. These data indicate that alpha 1-adrenergic receptors located in the central nervous system, inhibit in the dog tonic and stimulated GH secretion.

Animals↗
PubMed1983

alpha2-Adrenergic stimulation enhances growth hormone secretion in the dog: a presynaptic mechanism?

Intravenous administration of clonidine (CLO), (2,4 and 8/micrograms/Kg), a predominantly alpha 2-adrenergic receptor agonist, induced in unanesthetized dogs clear-cut and dose-related rises in plasma GH (cGH) levels. Pretreatment with the selective antagonist of alpha 1-adrenergic receptors prazosin (0.1 mg/Kg iv) left unaltered the cGH rise induced by 4/micrograms/Kg of CLO whilst blockade of alpha 2-adrenergic receptors by yohimbine (2.5 mg/Kg iv) completely prevented it. In dogs treated 24 h previously, with reserpine (0.5 mg/Kg iv), a depletor of brain catecholamine stores, CLO was ineffective to stimulate cGH release. These data indicate that in the dog the GH-releasing effect of CLO occurs via stimulation of alpha 2-adrenergic receptors and suggest that the latter are located presynaptically in relation to norepinephrine neurons.

Animals↗
PubMed1983

Prolactin lowering effect of amphetamine in normoprolactinemic subjects and in physiological and pathological hyperprolactinemia.

The effect on plasma prolactin (PRL) of d-amphetamine (Amph) was studied in normo- and hyperprolactinemic subjects. In normoprolactinemic women Amph failed to lower plasma PRL levels when infused intravenously over 1 h at the dose of 7.5 mg, but induced at the dose of 15.0 mg a modest inhibition of plasma PRL (maximum PRL inhibition 20 +/- 4.5% at 45 min). Likewise, in puerperal women Amph at the dose of 7.5 mg did not decrease significantly plasma PRL levels but it was active in this respect (maximum inhibition 37 +/- 10% at 120 min) at the dose of 15.0 mg. In subjects with presumptive evidence of a PRL-secreting adenoma, Amph at either the 7.5 mg or the 15.0 mg dose failed to alter baseline PRL levels. These results indicate that Amph is a poor PRL suppressor in either normo- or hyperprolactinemic subjects. It is proposed that this may be due to the drug's ability to effect release of dopamine mainly from a non-granular pool of the amine.

Adenoma↗
PubMed1983

Effect of agonists and antagonists of cholinergic neurotransmission on growth hormone release in the dog.

In unanaesthetized dogs iv administration of the cholinesterase inhibitor eserine (0.5 mg) or the cholinergic muscarinic receptor agonist oxotremorine (0.25 mg) induced a clear-cut rise in plasma canine growth hormone (cGH) levels. Complete suppression of the GH-releasing effect of eserine and oxotremorine was induced by blockade of cholinergic muscarinic receptors by atropine (80 or 20 micrograms/kg, 30 min before) but not by scopolamine-N-butyl bromide (0.8 mg/dog, 30 min before), an anticholinergic drug which does not cross the blood brain barrier (BBB). In contrast, activation of cholinergic nicotinic receptors by nicotine (6 mg) failed to alter resting cGH concentrations, and pre-treatment with the nicotinic receptor blocker mecamylamine (5 mg, 30 min before) did not counteract the GH-releasing effect of eserine. Other cholinomimetic drugs, e.g. pilocarpine, 4-aminopyridine, carbachol and bethanechol failed to induce a rise in plasma cGH concentrations. These data indicate that: 1) cholinergic muscarinic but not nicotinic receptors located in the central nervous system (CNS) inside the BBB play a facilitatory role in tonic cGH release; 2) pharmacologically distinct muscarinic receptors may exist in the CNS.

Animals↗
PubMedDate not supplied

Synthetic hpGRF 1-40 stimulates growth hormone and inhibits prolactin secretion in normal children and children with isolated growth hormone deficiency.

Intravenously administered synthetic hpGRF 1-40 at doses of 0.1, 0.33 and 1.0 microgram/kg increased plasma GH in a dose-dependent fashion in 4 normal prepubertal children. hpGRF 1-40 at the dose of 1.0 microgram/kg stimulated GH release, though to a lesser extent than in normals, in 7 children with isolated GH-deficiency (IGHD) but failed to do so in a patient with craniopharyngioma. In all normal children and 6/7 patients with IGHD, hpGRF 1-40 at all doses used induced a clear and sustained lowering of plasma prolactin levels; this effect was lacking in the patient with craniopharyngioma. hpGRF 1-40 had no effect on plasma FSH, LH, TSH or glucose levels nor did it influence pulse rate, blood pressure, or body temperature. These results indicate that hpGRF 1-40 is a potent stimulus to GH release in normal prepubertal children and holds promise for treatment of GH-deficient children. In addition, in both normal children and children with IGHD, hpGRF 1-40 is a potent suppressor of prolactin levels.

Adolescent↗