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Biomedical subjects

V Locatelli

Publications and source records attributed to V Locatelli.

At least 145 records · Page 8Linked to original sources
PubMed1979

Interaction between the thyrotrophin-releasing hormone-induced growth hormone rise and dopaminergic drugs: studies in pathologic conditions of the animal and man.

A rise in plasma growth hormone (GH) after thyrotrophin-releasing hormone (TRH) and a striking reduction after dopaminergic drugs is present in acromegalic ('responder') patients. We have investigated the GH response to dopaminergic stimuli in two conditions of animals and man, which, like acromegaly, are characterized by a TRH-induced GH rise, i.e. rats with electrolytic lesions of the median eminence (ME) and patients with hepatic cirrhosis. In addition, we have studied the TRH-induced GH rise in rats with ME lesions, in the cirrhotic patients and in a group of 'responder' acromegalics before and after administration of dopaminergic drugs. In rats with ME lesions an infusion of dopamine (DA) neither modified baseline GH levels nor the TRH-induced GH rise. In five out of six cirrhotic patients oral administration of L-Dopa was followed by the usual rise in plasma GH. infusion of DA increased plasma GH levels in three out of seven cirrhotic patients and in four out of five subjects an earlier GH rise after TRH was seen. However, in the 'responder' acromegalics, the infusion of DA, besides lowering baseline plasma GH, was capable of reducing the TRH-induced GH rise. Collectively these data indicate that the TRH-induced GH rise emphasizes defects in the neurohormonal links between the central nervous system and the anterior pituitary. Instead, the paradoxical fall of GH after dopaminergic drugs appears to be a prerequisite of acromegaly and may be attributable to receptors for DA located on the tumorous tissue.

Acromegaly↗
PubMed1979

Ultrastructure of somatotrophs of rats with median eminence lesions: studies in basal conditions and after thyrotropin-releasing hormone stimulation.

Anterior pituitaries from female Sprague-Dawley rats (160-200 g b.w) bearing electrolytic lesions of the median eminence were qualitatively and quantitatively investigated by electron microscopy and the findings compared with those from intact animals or sham-operated controls. This study was performed in basal conditions and after stimulation with thyrotropin-releasing hormone. Animals with lesions showed a reduction of both the number of somatotrophic cells and growth hormone granules. After injection of thyrotropin-releasing hormone exocytosis of growth hormone granules from somatotrophs was frequent in rats with lesions of the median eminence but rare in sham-operated animals. The differences were statistically significant.

Animals↗
PubMed1978

Prolactin and growth hormone releasing activity of [D-Met2, Pro5]-enkephalinamide in the rat after systemic administration.

The growth hormone (GH) and prolactin releasing (PRL) activity of [D-Met2, Pro5]-enkephalinamide (EKNH2). an opioid peptide analog with higher opiate agonist activity that morphine, was compared in the unanesthetized male rat to those of equimolar doses of morphine upon systemic injection. EKNH2 proved to be a higher PRL, but not GH, releaser than the opiate alkaloid.

Animals↗
PubMed1978

Pituitary hormones and ergot alkaloids.

From the data presented it appears that ergot drugs are both a useful tool for use in the study of neuroendocrine control of pituitary hormone secretion and a valid pharmacologic weapon for treatment of hyperprolactinemic states, GH and, probably, ACTH and MSH hypersecretion. In fact, they are capable of a long-lasting disruption of PRL secretion from a normal or tumoral pituitary gland, are unable to affect directly the somatotrophs of an intact AP, but inhibit GH and, possibly, ACTH secretion from a hyperplastic or tumoral gland. Ergolines also exert clear-cut PRL-lowering effects and are capable of suppressing GH secretion in acromegaly. The intimate mechanism(s) and hence site(s) of action of some of these compounds await clarification.

Acromegaly↗
PubMed1978

[The endocardial ventricular activation map in a case of intermittent BBS in phase III (author's transl)].

To obtain information on endocardial activation-sequence, unipolar recordings at seven left ventricular and six right ventricular points were performed in a 37-year-old man suffering from cardiomyopathy and tachycardia-dependent left bundle branch block (LBBB). Results were as follows: 1) the recovery time was longer in anterior than in posterior portion of left bundle branch fibers; 2) an high posterior left ventricular point was directly activated via posterior left bundle branch fibers; 3) the directly activated left ventricular zone was too small and relatively too late excited in respect of the right interventricular septum, from which the stimulus reached the left septum, to mask the LBBB electrocardiographic pattern; 4) in the presence of tachycardia-dependent LBBB the duration of left ventricular endocardial activation was about twice (62 msec) that found in the absence of tachycardia-dependent LBBB (28 msec).

Adult↗
PubMed1978

[Observations on the sequence of endocardial activation in the left ventricle of the normal subject].

To obtain information on normal left ventricular activation, endocardial recordings with an electrode catheter were made a seven left ventricular sites in ten patients undergoing diagnostic heart catheterization. All the patients had: 1) sinus rhythm; 2) normal duration and shape of the QRS complex of left chest leads; 3) normal left ventriculography, i.e. normal volume and contractility of the left ventricle. The earliest left ventricular endocardial activation was recorded at septal and/or posterior level, i.e. at the septum (6 to 16 msec, average 9.7 msec, after the onset of intracardiac QRS complex) in seven patients; at the posterior wall (0 to 4 msec, average 2.6 msec, after the onset of intracardiac QRS complex) in three patients (in one of these, the earliest activation occurred at the posterior wall and apex simulaneously). If the earliest activation occurred at the left interventricular septum, the next excited point was found on the posterior wall or at the apex, and vice versa. The latest part to be activated was on the lateral free wall in seven patients; on the posterior wall in two patients; at the apex in the last one.

Adult↗
PubMed1977

Effect of 5-hydroxytryptophan on prolactin and growth hormone release in the infant rat: evidence for different neurotransmitter mediation.

In 10 day-old female and male rats, administration of 5-hydroxytryptophan (5-HTP) induced a prompt elevation in plasma prolactin (Prl) and growth hormone (GH) levels. Pretreatment with 2 serotonin (5-HT) receptor blockers, methysergide (Meth) and metergoline (MCE), markedly reduced the 5-HTP-induced Prl rise but failed to alter the GH response to 5-HTP. Administration of 2 selective inhibitors of presynaptic 5-HT reuptake, 3-(p-trifluoromethylphenoxy)-N-methyl-3-phenyl-propylamine and chlorimipramine (CIM), potentiated the 5-HTP-stimulated Prl rise but significantly reduced the 5-HTP-induced GH release. Blockade of dopaminergic or alpha-adrenergic receptors by pretreatment with pimozide (Pim) or phentolamine (Phent), respectively, or central sympathectomy by intraventricularly (i.vt.) injected 6-hydroxydopamine (6-OHDA) were capable of reducing the 5-HTP-induced GH release without affecting the 5-HTP-induced Prl rise. These data indicate that in the infant rat the 5-HTP-induced Prl release is mediated via the brain 5-HT system and that a nonspecific activation of the catecholaminergic system is responsible for the GH response to the drug.

5-Hydroxytryptophan↗
PubMed1977

Thyrotrophin releasing hormone-induced growth hormone and prolactin release: physiological studies in intact rats and in hypophysectomized rats bearing an ectopic pituitary gland.

To determine how the sensitivity of the ectopic anterior pituitary gland to the GH-releasing effect of thyrotrophin releasing hormone (TRH) might be affected by the time lapse from transplantation, TRH (0-15 and 0-6 microng) was injected i.v. into hypophysectomized (hypox)-transplanted rats under urethane anaesthesia 1,3,8,15,30 and 60 days after transplantation, and plasma samples were taken 5 and 10 min later. Baseline GH values gradually decreased with time from about 16-0 ng/ml (1 day) to about 3-0 ng/ml (30 and 60 days). The TRH-induced GH release was absent 1 day after transplantation, present only with the higher TRH dose 3 and 8 days after transplantation, and clearly elicitable, also with the lower TRH dose (0-15 microng), from 15 up to 60 days. Determination of plasma prolactin concentrations showed a decline from about 85-0 ng/ml (1 day) to about 32-0 ng/ml (8 days); subsequently (15-60 days) prolactin values stabilized. Plasma prolactin levels increased 15 and 60 days after transplantation only when a dose of 0-6 microng TRH was given. In intact weight-matched rats, TRH induced a GH response only at the dose of 1-2 microng while a short-lived but clear-cut prolactin response could be obtained even with the 0-3 microng dose. The present results indicate that: (1) disconnexion between the central nervous system and the anterior pituitary gland greatly enhances GH responsiveness while blunting prolactin responsiveness to TRH; (2) the sensitivity of the anterior pituitary gland to the GH-releasing effect of TRH increases with time from transplantation; (3) TRH is a more effective prolactin- than GH-releaser on the pituitary gland in situ.

Animals↗