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Biomedical subjects

C Bellido

Publications and source records attributed to C Bellido.

At least 91 records · Page 5Linked to original sources
PubMed1985

Prepuberal reproductive defects in neonatal estrogenized male rats.

Intact Wistar male rats injected on Day 1 with 500 micrograms of estradiol benzoate or olive oil were decapitated on Days 15 and 22 or maintained until adulthood to analyze the balanopreputial separation. Other oil or estradiol-treated rats were orchidectomized on Day 15 and decapitated on Day 22. The neonatal estrogenization produced the following reproductive changes prior to puberty: testis, adrenal, and ventral prostate atrophy; increase in the weights of seminal vesicles and epididymis; decrease in testosterone plasma levels; delayed balanopreputial separation; abolition of luteinizing hormone response to orchidectomy; transient increase in prolactin plasma levels; and blockade in seminal and prostate response to orchidectomy.

Adrenal Glands↗
PubMed1985

[Effect of pargyline on the response to CO2 stress].

The effects of pargyline administration during three days on male rats for stress reaction caused by hypercapnia, taking into account the contents of noradrenaline in the left auricle, the right auricle, the ventricle, the spleen and the hypothalamus have been studied. The stress by CO2 only produces a significant depletion of noradrenaline at the hypothalamus level. The administration of pargyline (50 mg/kg/day) induces significant increases in the content of noradrenaline in all the tissues. The increases in noradrenaline content are greater when the pargyline is given before the stress.

Animals↗
PubMed1985

Effects of pimozide and domperidone administration on prolactin levels in neonatally estrogenized female rats.

The effects of two dopaminergic blockers, pimozide and domperidone, on the prolactin secretion were investigated in adult female rats treated neonatally with estrogens (100 micrograms of estradiol benzoate s.c. on day 1). These rats showed hyperprolactinemia (556 micrograms/l vs 57.7 in oil-injected) and treatment with pimozide or domperidone failed to increase prolactin levels in the adult age. These results suggest that the hyperprolactinemia in neonatally estrogenized female rats is produced by loss of the dopaminergic inhibition on prolactin secretion, so that the pharmacological blockade of dopaminergic receptors is uneffective. The dopamine levels in hypothalamus were similar in control and estrogenized females suggesting that failure in dopaminergic inhibition is due to a decrease in dopamine secretion to portal vessels.

Animals↗
PubMed1982

Cyproheptadine-induced remission of Cushing's disease due to pituitary basophil adenoma.

Serotonin is involved in the control of ACTH secretion, possibly by stimulating corticotropin releasing factor secretion from the hypothalamus. Cushing's disease seems to be due to defective hypothalamic regulation of ACTH release from the pituitary gland. Cyproheptadine is a potent antagonist of serotonin and has been used successfully in some patients with Cushing's disease, although, generally, in women without radiological evidence of pituitary tumors. We report the successful use of cyproheptadine in a 54-year-old man with Cushing's disease due to pituitary basophil adenoma. Significant clinical and biochemical improvement was noted 45 days after treatment began. The results in this patient support our findings that cyproheptadine can be effective in patients with Cushing's disease due to pituitary tumors, as well as in preparing very ill patients for surgery or managing such patients until radiotherapy takes effect.

Adenoma, Basophil↗
PubMed1981

[Changes in the expression of H-2 antigenic determinants in several sublines proceeding from the same tumor].

Four sublines of the chemically induced BALB/c tumour MCG4 have been obtained after serial intraperitoneal transplantation in syngeneic recipients and have been named MCG4-O, MCG4-A, MCG4-B and MCG4-C. The four subline have been typed for H-2 antigens in a complement dependent microradioassay with H-2 alloantisera defining H-2 specificities as well as with two syngeneic anti tumour sera: BALB/c anti MCG4-O and BALB/c anti MCG4-A. The results obtained showed a progressive loss of the foreign H-2 antigens detected in the primitive line, MCG4-O, with a simultaneous appearance of the appropriate H-2 antigens detected in MCG4-B and MCG4-C. Furthermore the immunogenic capacity of the sublines decrease progressively with the transplantation procedures, rendering MCG4-O and MCG4-A highly immunogenic and capable of producing isoantibodies while MCG4-B and MCG4-C are poorly immunogenic. The results could suggest that the primitive subline is heterogeneous mixture of (H-2d) are immunoselected by the transplantation procedures with rejection of the most immunogenic clones, which would express the foreign H-2 antigens.

Animals↗
PubMed1981

Immunocomplexes and tumour growth. Detection of immunocomplexes in high and low malignant tumour sublines.

Two different techniques to measure immunocomplexes on biological fluids are presented. The first one is based on the inhibition of the antibody dependent cell cytotoxicity (ADCC). A competition is established between immunocomplexes and the rabbit anti chicken antibodies bound to chicken red blood cells for the Fc receptors of K cells. The second technique detects the presence of immunocomplexes by the inhibition of the cytotoxicity on a haemolytic system as a result of the consumption of the complement. Both techniques were performed in parallel to compare their sensitivity. The presence of immunocomplexes in the ascites of tumour bearing mice has been demonstrated with two highly related tumours (MCG4 O and MGC4 C) with different immunogenic properties. No immunocomplexes were detected in the serum of the same mice.

Animals↗
PubMedDate not supplied

Mast cells in the testis, epididymis and accessory glands of the rat: effects of neonatal steroid treatment.

Mast cells in the testis of control adult rats were found almost exclusively around subcapsular blood vessels. Discrete mast cells were distributed throughout the stroma of the epididymis and sex accessory glands. In neonatally estrogen-treated rats, a greater number of mast cells was present in the testicular interstitium, whereas no significant increase in the number of mast cells per square millimeter of stroma was found for the epididymis and sex accessory glands, despite stromal proliferation. On the other hand, androgen-treated rats did not have increased mast cell numbers in any organ. These results indicate that the increase in mast cell numbers was estrogen-dependent, specifically related to the testis and did not seem to be a consequence of the increase in the connective interstitial tissue.

Animals↗
PubMedDate not supplied

A possible dual mechanism of the anovulatory action of antiprogesterone RU486 in the rat.

The purpose of these experiments was to investigate the mechanism of the anovulatory action of antiprogesterone RU486 (RU486) in rats by studying its effects on follicular growth, secretion of gonadotropins and ovarian steroids, and ovulation. Rats with 4-day estrous cycles received injections (s.c.) of either 0.2 ml oil or 0.1, 1, or 5 mg of RU486 at 0800 and 1600 h on metestrus, diestrus, and proestrus. At the same times, they were bled by jugular venipuncture to determine serum concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), 17 beta-estradiol (E), and progesterone (P). On the morning of the day after proestrus, ovulation and histological features of the ovary were recorded. Rats from each group were killed on each day of ovarian cycle to assess follicular development. Rats treated similarly were decapitated at the time of the ovulatory LH surge and blood was collected to measure LH. The serum levels of LH increased and those of FSH decreased during diestrus in rats treated with RU486. Neither E nor P levels differed among the groups. Treatment with RU486 caused both a blockade of the ovulation and an increase in ovarian weight in a dose-dependent manner. At the time of the autopsy (the expected day of ovulation), rats treated with 1 mg RU486 had ovaries presenting both normal and post-ovulatory follicles and unruptured luteinized follicles. Rats treated with 5 mg RU486 presented post-ovulatory follicles without signs of luteinization. The number of follicles undergoing atresia increased in rats treated with RU486. Rats treated with 5 mg RU486 exhibited a significant decrease in ovulatory LH release. The mechanism by which RU486 produces the ovulatory impairment in rats seems to be dual: first, by inducing inadequate follicular development at the time of the LH surge and second, by reducing the amount of ovulatory LH released. The physiological events-decreased basal FSH secretion and follicular atresia-that result from use of RU486 cannot be elucidated from these experiments and should be investigated further.

Animals↗
PubMedDate not supplied

LH response to LH-RH neonatally estrogenized male rats.

The LH response to 100 or 1000 ng of LH-RH was studied in adult male rats treated neonatally with 500 micrograms of estradiol benzoate or olive oil. The dose of 100 ng elicited the same LH increase in both groups, but the estrogenized animals responded more when 1000 ng of LH-RH was injected. These data suggest that the decreased LH response to orchidectomy found in estrogenized animals is not due to a failure in pituitary responsiveness to LH-RH.

Animals↗
PubMedDate not supplied

Mechanisms in the production of prepuberal reproductive defects in neonatal estrogenized male rats.

Neonatal estrogenization induced in prepubertal males atrophy of the testis and ventral prostate and increased the weight of the seminal vesicles. Atrophy of the testis was probably due to the inhibition of FSH and LH secretion: males estrogenized on day one and sacrificed daily from day six to day fifteen showed lower gonadotropin levels than their respective controls. In addition, daily FSH and LH administration (80 micrograms/100 g BW and 40 micrograms/100 g BW respectively) from day one to day fifteen increased testicular development more effectively in estrogenized than in control males and the differences between the two groups disappeared. Prostate atrophy was due to the decreased testosterone secretion. The reason for the hypertrophy of the seminal vesicles remains unclear: reduction in Prolactin levels due to bromocriptine treatment did not normalize the seminal vesicles weight, indicating that hyperprolactinemia was not the cause. Male rats estrogenized on day one, orchidectomized on day 5 and decapitated on day fifteen also showed hypertrophy in their seminal vesicles. These results indicate that testicular factors, other than testosterone, were not responsible for the vesicular hypertrophy. It seem possible that estrogens might act directly on vesicular growth.

Adrenal Glands↗
PubMedDate not supplied

Response of testicular macrophages to EDS-induced Leydig cell death.

The response of testicular macrophages to massive Leydig cell death was studied by the administration of the specific Leydig cell cytotoxic ethylene dimethane sulphonate (EDS) to sham-operated (SO), short-term (STHX), and long-term (LTHX) hypophysectomized rats. EDS-killed Leydig cells showed the morphological features of the programmed cell death or apoptosis. A 2-fold increase in the number of macrophages was found on days 1-2 after treatment in both SO and STHX rats, and dead Leydig cells were completely eliminated by day 3 after treatment. Otherwise, in LTHX rats, there was a delay in the increase in the number of macrophages, and EDS-killed Leydig cells remained in the testicular interstitium for several days. These results indicate that the phagocytic capacity of the macrophage population was diminished in hypophysectomized rats, and particularly after long-term hypophysectomy.

Animals↗
PubMedDate not supplied

Response of the testis to gonadotrophin replacement in young hypophysectomized vs. gonadotrophin-releasing hormone antagonist-treated rats.

We have studied the response of atrophic Leydig cells to gonadotrophin replacement in young hypophysectomized (HX) and GnRH antagonist (GnRH-ANT)-treated rats. Hypophysectomy was performed at 28 days of age. Age-matched rats were treated with GnRH-ANT from 28 to 51 days of age. From 45 to 51 days of age, animals were injected with 5 IU recFSH, 10 IU hCG or vehicle. Body and testicular weights, as well as the diameter of the seminiferous tubules were significantly higher in GnRH-ANT-treated than in HX rats. Both recombinant FSH and hCG treatments induced a similar increase in testicular weight and tubule diameter in HX and GnRH-ANT-treated rats. However, hCG treatment induced a significantly higher increase in Leydig cell size in HX (3.2-fold) than in GnRH-ANT-treated (1.4-fold) rats. These results suggest that the response of atrophic Leydig cells to gonadotrophin supplementation was partially inhibited in the presence of GnRH antagonist, whereas Sertoli cell-mediated responses seem not to be affected.

Animals↗
PubMedDate not supplied

Simultaneous proliferation and differentiation of mast cells and Leydig cells in the rat testis. Are common regulatory factors involved?

The proliferation and differentiation of mast cells and Leydig cells were studied in adult sham operated or hypophysectomized rats after the administration of ethylene dimethane sulphonate (EDS) and in prepubertal rats after neonatal treatment with a gonadotropin-releasing hormone (GnRH) antagonist (Organon 30276; Oss, The Netherlands). After treatment with EDS, two proliferative waves were found. On day 3, several interstitial cell types proliferated, whereas mitotic cells corresponded to differentiating Leydig cells and mast cells around day 20. Differentiating Leydig cells showed a higher mitotic index than that of differentiating mast cells. Hypophysectomized animals showed high mitotic activity 3 days after treatment, but 21 days after treatment differentiating Leydig cells were absent and proliferative activity was reduced. The number of mast cells increased from day 15 to day 30 in EDS-treated rats and from day 15 to day 50 in hypophysectomized, EDS-treated rats. GnRH antagonist-treated rats showed poorly differentiated Leydig cells and abundant mitotic figures on day 23. Proliferation and differentiation of Leydig cells occurred concomitantly with the proliferation and differentiation of mast cells between 23 and 30 days of age. These results suggest that Leydig cells and mast cells in the rat testis share some common regulatory factors.

Animals↗
PubMedDate not supplied

Balano-preputial separation as an external sign of puberty in the rat: correlation with histologic testicular data.

In order to correlate the date of balano-preputial separation (BPS) with the testicular development, twenty four rats were selected from an experimental design focused on the effects of pituitary grafts on puberty. Animals that presented BPS at an early age, showed a smaller volume of the seminiferous epithelium and a lower spermatogenic level than that presented BPS at a more advanced age. These data indicate that the advancement in BPS induced by pituitary grafts was not in keeping with an equivalent enhancement of testicular development.

Analysis of Variance↗
PubMedDate not supplied

Differences in prepuberal neonatally estrogenized or androgenized male rats.

The main objective of this work was to analyze the different effects produced in prepuberal male rats by neonatal androgenization or estrogenization. For this purpose male Wistar rats were injected on day one of life with 500 micrograms of estradiol benzoate (estrogenized animals), 500 micrograms of testosterone propionate (androgenized animals) or olive oil (control animals) and decapitated on day 15. At the moment of decapitation estrogenized animals showed decreases in body, testes, prostate and adrenal weights, increases in pituitary, seminal vesicles and epididymis weights, an increase in prolactin plasma levels and a decrease in those of androgens. Androgenized animals showed only decreased testes and epididymis weights and androgen plasma levels. These results evidence the presence of important qualitative differences in prepuberal neonatally estrogenized or androgenized rats, especially in the accessory sex organs.

Adrenal Glands↗