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Biomedical subjects

D Cocchi

Publications and source records attributed to D Cocchi.

At least 163 records · Page 9Linked to original sources
PubMed1976

Stimulation of growth hormone release by luteinizing hormone-releasing hormone and melanocyte-stimulating hormone-release inhibiting hormone in the hypophysectomized rat bearing an ectopic pituitary.

Intrajugular administration of LHRH (0-6 and 1-2 mug) in hypophysectomized rats which received renal grafts of anterior pituitary induced a small but significant rise in plasma GH 5 and 10 min post-treatment. LHRH, at the same dose levels, was ineffective in weight-matched intact controls. MIF, at the dose of 1-2 mug, induced a slight GH rise 5 min after treatment in hypophysectomized trasnplanted rats, while it was ineffective in intact controls. Unlike the two hypothalamic peptides, alpha-MSH (0-6 and 1-2 mug) was ineffective as a GH-releaser in both transplanted and intact rats.

Animals↗
PubMed1976

Altered growth hormone and prolactin responsiveness to TRH in the infant rat.

12-day-old female and male pups were killed 10 min after the injection of either saline or thyrotropin releasing hormone (TRH), and plasma growth hormone (GH) and prolactin (PRL) levels were measured by radioimmunoassay (RIA). At all doses used (0.15, 0.3, 0.6 and 1.5 mug/100 g b.w.i.p.), TRH induced a significant, although not dose-related, increase in plasma GH levels, but was effective in releasing PRL only at the greatest dose level (1.5 mug/100 g b.w.). The GH-releasing effect of TRH was even more evident in 12-day-old pups subjected to central sympathectomy of 6-hydroxydopamine (6-OHDA, 60 mug/10 mul intraventricular route) 1 week before; in these animals, TRH was ineffective in releasing PRL even at the greatest dose level (1.5 mug/100 g b.w.). In pups pretreated with 6-OHDA, the GH-lowering effect of insulin hypoglycemia or cold exposure was markedly reduced, while the PRL responses were unmodified. Baseline plasma PRL levels were markedly increased following 6-OHDA administration. It is proposed that in the infant rat the greater GH than PRL responsiveness to TRH, which opposed the pattern of response present in the adult animal, may be due to the existence of a 'physiologic' functional disconnection between the central nervous system (CNS) and the anterior pituitary (AP). Results obtained following central sympathectomy by 6-OHDA, which further disrupted CNS-AP links, substantiate this view.

Animals↗
PubMed1976

Stimulation of growth hormone release by thyrotropin-releasing hormone in the hypophysectomized rat bearing an ectopic pituitary.

Hypophysectomized female rats which received renal grafts of anterior pituitary (AP) or weight-matched intact controls were sampled under urethane anesthesia. Plasma growth hormone (GH) in sequential samples from each rat was measured by radioimmunoassay to determine the effect of exogenous thyrotropin-releasing hormone (TRH) on GH release from ectopic or intact AP. In a first experiment, following a baseline sample, a pre-treatment sample was taken from each rat 30 min after urethane injection, after which TRH (0.3 or 0.6 mug) or isotonic saline was injected iv, and samples were taken at 10 and 30 min post-treatment. Baseline GH levels in hypophysectomized-transplanted rats were in the range of 4.0 to 8.0 ng/ml, and were not modified significantly by urethane. TRH caused a significantly greater increase in growth hormone at 10 min than did saline. Plasma GH tended to be higher at 30 min post-treatment only in the 0.6 mug TRH-treated group. In further experiments the above described protocol was followed except that four doses of TRH were used (0.15, 0.3, 0.6, and 1.2 mug) and post-TRH blood samples were taken at 5 and 10 min. TRH caused a clear-cut increase in plasma GH both at 5 and 10 min, although no dose-effect relationship was present. In intact controls, baseline GH levels were in the range 40.0 to 80.0 ng/ml and were drastically reduced by urethane. In these animals, only the 1.2 mug TRH dose induced a GH rise at 5 and 10 min. In similar experiments, iv administration of vasopressin (100, 200, or 400 mU) induced a rise in plasma GH when given to the hypohysectomized-transplanted rats, but was ineffective in intact controls; the administration of prostaglandin E2 (5.0 and 50.0 mug) increased plasma GH in both experimental conditions. The results indicate that TRH in the hypophysectomized-transplanted rat acts directly on the AP tissue to increase GH release and that the ectopic pituitary is more susceptible than the in situ pituitary to some GH-releasing stimuli.

Animals↗
PubMed1975

Hyporesponsiveness to glucoprivation during postnatal period in the rat.

2-Deoxy-D-glucose (2-DG), a glucose analogue, blocks glycolysis and induces intracellular glucoprivation. In the adult rat intraperitoneal administration of 2-DG or its injection into the lateral ventricle (IVT) of the brain induces hyperglycemia which is divorced from a rise in plasma insulin (IRI). In the present study, responsiveness to 2-DG-induced glucoprivation, after central or intraperitoneal injection of the drug, was studied in rats of 7, 14, 21, and 28 days of age and compared to that of the adult rat (50 days old). In 7-, 14-, 21-, and 28-day-old rats, the overall blood glucose (BG) response to IVT-injected 2-DG was equivalent to 4, 3.3, 17, and 33%, respectively, of the BG response present in the adult rat. Following intraperitoneal injection of 2-DG , the BG response evoked in the same age groups corresponded to 27, 31, 41, and 93%, respectively, of the adult response. Base-line plasma IRI levels were significantly lower in pups than in adults and increased progressively with age, but no difference was present in IRI levels between 2-DG-treated and control pups whether the 2-DG was given via the laterl ventricle or intraperitoneally. These results demonstrate the presence in the infant rat of clear-cut hyporesponsiveness to 2-DG-induced glucoprivation. The different response pattern between experiments involving central and peripheral 2-DG administration supports the existence of separate peripheral glucoreceptors for 2-DG and their earlier ontogenic activation. Since the infant mammal glucose is of minor relevance as an energy substrate, an interrelationship appears to be present between requirements for fuel(s) and homeostatic response to fuel deprivation.

Age Factors↗
PubMed1975

Effect of hypophysectomy and growth hormone on tryptophan and serotonin metabolism.

The present study reports data on brain serotonin (5-HT) metabolism in two experimental conditions which have in common a lack of pituitary growth hormone (GH) and refers also the effect of a GH replacement therapy. In hypophysectomized female rats or genetically dwarf mice, which have a more selective deficiency of GH, brain tryptophan (TP) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations were significantly higher than in age-matched controls. Brain levels of 5-HT were practically unchanged. A GH replacement therapy resulted in both hypophysectomized rats and dwarf mice in a significant reduction of brain TP and 5-HIAA concentrations. These results suggest that GH may exert an inhibitory action on 5-HT metabolism. Consonant with this view are the preliminary findings that in 7 individuals with elevated plasma GH levels for acromegaly, plasma TP levels were lower than in control subjects.

Acromegaly↗