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Biomedical subjects

A Gomez-Pan

Publications and source records attributed to A Gomez-Pan.

47 records · Page 3Linked to original sources
PubMed1975

Growth hormone release inhibiting hormone: actions on thyrotrophin and prolactin secretion after thyrotrophinreleasing hormone.

The hypothalamic tetradecapeptide growth hormone release inhibiting hormone (GH-RIH) blocked the thyrotrophin response to thyrotrophin-releasing hormone (TRH) in normal people and in patients with primary hypothyroidism. This inhibition was dose related. The TRH-induced prolactin release was not affected by GH-RIH. This dissociation of the thyrotrophin and prolactin responses to TRH by GH-RIH suggests that there are different mechanisms for release of thyrotrophin and prolactin and that only the former is affected by GH-RIH.

Adult↗
PubMed1975

Direct inhibition of gastric acid and pepsin secretion by growth-hormone release-inhibiting hormone in cats.

Growth-hormone release-inhibiting hormone (G.H.-R.I.H.) inhibited gastric acid and pepsin secretion in response to pentagastrin and food stimulation in cats. This effect is mediated by a direct action on the parietal and peptic cells. No evidence of a post-inhibitory acid or pepsin secretory rebound was obtained. Thus a compound of hypothalamic origin can exert a direct effect on exocrine secretion. In view of its widespread actions and its presence in relatively high concentrations in various organs apart from the hypothalamus, G.H.-R.I.H. might also be regarded as a factor responsible for local coordination of endocrine and exocrine secretion.

Animal Feed↗
PubMed1975

The mechanism whereby growth hormone-release inhibiting hormone (somatostatin) inhibits food stimulated gastric acid secretion in the cat.

Growth hormone-release inhibiting hormone (somatostatin) inhibits the gastric acid response to food in concious cats. We have confirmed that this tetradecapeptide blocks the food stimulated gastrin release. However, the inhibition of gastrin release is delayed relative to that of acid secretion, &howing that the inhibition of food stimulated acid secretion is by primary effect on the acid secretory mechanism. No evidence was found of potentiation of either the gastric acid output or serum concentration of gastric in response to food.

Animals↗
PubMed1975

Hypothalamic hormone interaction in acromegaly.

The growth hormone response to the administration of the currently available synthetic hypothalamic hormones was assessed in eleven patients with acromegaly. Eight of them showed a positive GH response to thyrotrophin releasing hormone and three showed no response. The GH response to TRH was shown to be unrelated to the thyrotrophin response to TRH. The GH response to TRH was inhibited by the administration of growth hormone release inhibiting hormone. Luteinizing hormone/follicle stimulating hormone releasing hormone (LHRH) caused a positive GH response in four patients, but this was trivial in three. The TRH mediated GH release in acromegaly is not mediated via TSH and appears to be attributable to loss of specificity of the receptor sites on the somatotroph to the hypothalamic hormones.

Acromegaly↗
PubMed1974

Pituitary-thyroid function in Pendred's syndrome.

Pendred's syndrome is reported in three siblings. All were euthyroid, with large goitres and deaf mutism and all had an unusual deposition of pigment in the retina. All had raised circulating levels of triiodothyronine (T-3) and an exaggerated response of thyroid-stimulating hormone (TSH) to thyrotrophin-releasing hormone (TRH). It appears that their compensated euthyroid state was maintained by the raised T-3 levels. We suggest that preferential T-3 production is maintained by increased TSH secretion in subjects with intrathyroidal iodine deficiency secondary to thyroid organification defect.

Adult↗
PubMed1973

Luteinizing hormone and follicle stimulating hormone-releasing hormone test in patients with hypothalamic-pituitary-gonadal dysfunction.

A standard intravenous 100 mug luteinizing hormone/follicle stimulating hormone-releasing hormone (LH/FSH-RH) test was used to assess the pituitary gonadotrophin responses in 155 patients with a variety of diseases of the hypothalamic-pituitary-gonadal axis. In all but nine patients there was an increase in circulating levels of either LH or FSH in response to the releasing hormone though 137 (88%) were clinically hypogonadal. It was not possible with this test to distinguish between hypothalamic and pituitary causes of hypogonadotrophic hypogonadism, since a variety of LH and FSH responses emerged within the disease groups. However, primary gonadal failure characteristically resulted in exaggerated gonadotrophin response. The potential therapeutic use of the gonadotrophin releasing decapeptide is suggested in certain patients with hypogonadotrophic hypogonadism.

Adolescent↗