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Biomedical subjects

E Carro

Publications and source records attributed to E Carro.

25 records · Page 2Linked to original sources
PubMed1997

Retinoic acid inhibits in vivo thyroid-stimulating hormone secretion.

Retinoids are needed for normal growth and development. Retinoic acid (RA), an active metabolite of vitamin A, acts through nuclear receptors that belongs to the superfamily which also includes the T3 receptors and 1-25-dihydroxyvitamin D receptor. In order to assess whether RA is a regulator of in vivo thyroid-stimulating hormone (TSH) secretion, we studied the effect of RA administration on spontaneous basal TSH secretion and TSH responses to TRH in either euthyroid or hypothyroid rats. We found that rats treated with RA showed a decrease in spontaneous basal TSH levels and TSH responses to TRH. Similarly, RA administration to hypothyroid rats led to a decrease on TSH responses to TRH. Our data suggests that RA plays an important inhibitory role on in vivo secretion and this effect is unrelated to the thyroid status of the animals.

Animals↗
PubMed1997

Neuropharmacological assessment of growth hormone secretion.

The biochemical diagnosis of individuals who are either deficient in growth hormone (GH) or who have alterations in the normal pattern of GH secretion is difficult. The uncertainty surrounding diagnosis reflects the lack of a thorough understanding of the physiology of GH secretion and of the hypothalamic hormones involved. At least three hormones are implicated: GH-releasing hormone (GHRH), somatostatin and the endogenous ligand of the GH secretagogue receptor, although the role that each plays in the release of GH is not clear from the available experimental evidence. In such a situation, most of the dynamic tests of GH secretory capacity in humans need to undergo a 'trial and error' process before being validated. The search for the 'gold standard' test of GH secretion is ongoing, and the combination of GHRH plus GH secretagogues will probably play an important role in future clinical diagnosis.

Growth Hormone↗
PubMed1997

Influence of endogenous leptin tone on the estrous cycle and luteinizing hormone pulsatility in female rats.

Recent data indicate that leptin may well play an important regulatory role in the hypothalamo-pituitary-gonadal axis. In order to further unravel the mechanisms by which leptin acts, we have studied the effect of treatment (8 days) of leptin antiserum (5 microl daily; i.c.v.) on LH pulsatility and estrous cycle in adult female rats. The administration of leptin antiserum led to a marked decrease in LH pulsatility as assessed by the area under the curve (13.5 +/- 4.7 ng/ml) in comparison to rats treated with normal rabbit serum (114 f 53 ng/ml; p < 0.01). Furthermore, rats treated with leptin antiserum showed an impairment of reproductive function as shown by the fact that all rats remained in anestrus. In conclusion, these data show that leptin markedly influences LH secretion and the estrous cycle in the female rat.

Animals↗
PubMed1997

Regulation of in vivo growth hormone secretion by leptin.

Leptin, the product of the ob gene, is a recently discovered hormone secreted by adipocytes that regulates food intake and energy expenditure. Growth hormone (GH) secretion is markedly influence by body weight being markedly suppressed in obesity and underweight. The aim of the present study was to study whether leptin can act as a metabolic signal connecting the adipose tissue with the growth hormone axis. We administered leptin antiserum (10 ul, i.c.v.) or normal rabitt serum (NRS; 10 ul, i.c.v.) to freely moving fed rats. Furthermore we assessed the effect of leptin administration (10 ug, i.c.v.) on fed and fasted rats. Spontaneous GH secretion was assessed over 6 hours with blood samples taken every 15 min. Administration of leptin antiserum led to a decrease in spontaneous GH secretion as assessed by the area under the curve (AUC) (168+/-72 ng/ml/6h) in comparison to NRS-treated rats (813+/-179 ng/ml/6h, p<0.01). While leptin administration (10 ug/rat; i.c.v.) to normal fed rats did not modify spontaneous GH secretion, leptin administration to fasted rats led to a reversal of the inhibitory effect exerted by fasting on GH secretion (AUC, 1650+/-351 ng/ml/6h vs 77+/-32 ng/ml/6h, p<0.01). This data suggests that leptin is a metabolic signal that regulates GH secretion.

Activity Cycles↗
PubMed1994

Acute ethanol administration in diestrus-2 in the rat on pulsatile prolactin and LH release.

Exposure to ethanol is followed by changes in reproductive function in man and animals, characterized by modifications in the secretion patterns of prolactin and luteinizing hormone (LH). As both hormones are secreted in an episodic fashion, the present work was undertaken to study the effects of acute ethanol administration on pulsatile prolactin and LH secretion patterns in adult female rats. Rats were previously cannulated to allow a continuous blood withdrawal to study the pulsatile patterns of prolactin and LH. The mean values of prolactin during the bleeding period and the absolute pulse amplitude of prolactin peaks were significantly increased by acute ethanol administration, whereas a significant decrease of relative pulse amplitude and frequency of this hormone was observed. On the other hand, ethanol administration increased the mean serum LH levels and the absolute and relative amplitudes of LH peaks. Ethanol treatment did not modify either frequency or duration of LH peaks. These data suggest that acute ethanol administration in adult female rats is followed by changes in the pulsatile prolactin and LH secretory patterns, which might be part of the mechanism to explain ethanol effects on the endocrine system.

Animals↗
PubMed1981

Steroids in severe head injury: A prospective randomized clinical trial.

This is a prospective randomized study of the efficacy of steroid therapy in patients with severe head injury. One hundred patients were randomized into two equal groups: the steroid group received 5 mg/kg/day of methylprednisolone, and the nonsteroid group received no drug. The groups were similar in their clinical features. All patients received a standardized therapeutic regimen. The patients were also classified as early responders or nonresponders to the overall treatment protocol without regard to steroid administration, on the basis of change in Glasgow Coma Scale score during the first 3 days of admission. There was no statistically significant difference in the outcome of the steroid and nonsteroid group at 6 months. Of the responders who were on steroids, 74% had good outcomes or were disabled, compared with 56% of the responders who did not receive steroids. In the nonresponder group, the patients on steroids were actually associated with a worse outcome than those who did not receive steroids: 75% of the nonresponders who received steroids were dead or vegetative, compared to 56% of those who were not receiving steroids. The data suggest that: 1) the effect of steroids may be different for different patient groups; 2) in order to identify these patients, a sensitive coma scale is needed; and 3) a rational approach to steroid therapy in head-injured patients may be to start all patients on steroids, but to discontinue their use in patients identified as not benefiting from steroid therapy.

Adolescent↗