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Biomedical subjects

F Labrie

Publications and source records attributed to F Labrie.

At least 523 records · Page 29Linked to original sources
PubMed1982

Effect of GnRH-induced endogenous luteinizing hormone release and exogenous progestogen treatment on ovarian activity in the postpartum ewe.

In two experiments, 64 crossbred ewes that had lambed in September or January and had their lambs removed within 24 h after birth were assigned to four groups and given the following treatments: group 1 (16 ewes)-1 ml saline, im or iv on d 10 postpartum; group 2 (24 ewes)-150 microgram/gonadotropin releasing hormone (GnRH) in 1 ml saline, im or iv on d 10 postpartum; group 3 (16 ewes)-150 microgram/GnRH in 1 ml saline, im or iv on d 10 postpartum, plus 40 mg fluorogestone acetate (FGA)-impregnated intravaginal sponges for 12 d beginning 22 d postpartum and group 4 (eight ewes)-40 mg FGA-impregnated intravaginal sponges only for 12 d beginning 22 d postpartum. Pregnant mare's serum gonadotropin (500 IU) was injected im into FGA-treated ewes at the time of sponge removal. Blood samples were collected from eight ewes in groups 1 and 2 at regular intervals up to 2 and 6 h, respectively, after treatment and analysed for luteinizing hormone (LH). Plasma progesterone (P) levels in blood collected once or twice weekly were used to monitor ovarian activity. GnRH induced a release of LH in all ewes monitored, whereas the LH levels remained unchanged in saline-treated ewes. Only 44% of the latter ewes had shown evidence of luteal activity by 50 d postpartum. The mean plasma P levels in the GnRH-treated ewes did not rise above basal preinjection values during the 14 d after treatment. In contrast, a synchronized ovulation followed by normal luteal activity was induced in 88% of the FGA-sponge-treated ewes. Of 16 ewes from group 2 slaughtered 26 d postpartum, 13 had ovaries that contained luteinized structures and uterine involution was incomplete in six ewes. These results preclude the use of GnRH as a single injection for induction of cyclic ovarian activity in the early postpartum ewe and indicate the need for progestogen treatment to initiate cyclic ovarian activity by 35 d postpartum. However, incomplete uterine involution may limit the number of ewes that can be successfully rebred at this time.

Animals↗
PubMed1982

New hormonal therapy in prostatic carcinoma: combined treatment with an LHRH agonist and an antiandrogen.

In order to block the influence of androgens from all sources on the growth of prostatic cancer, we have used a new hormonal therapy based on medical castration achieved with the potent LHRH agonist [D-Ser(TBU)6, des-Gly-NH2(10)]LHRH ethylamide (HOE-766) combined with the administration of a pure antiandrogen that neutralizes the action of adrenal androgens as well as those still secreted in low amounts by the testis during LHRH agonist treatment. This study was performed in ten patients with advanced prostatic carcinoma (9 at stage D2 and one at stage C). Bone pain, prostatism and general well-being were 60 to 90% improved within one month after starting treatment in all patients. After 2 months of treatment, minimal bone pain remained only in one patient who was originally bedridden. Bone scanning showed a 70 to 90% decrease in uptake after 3 to 5 months of treatment in the patients studied. Acid phosphatase levels were 60 to 90% reduced after 2 months of treatment in 3 out of the 4 patients who had elevated levels before therapy. Marked objective and subjective improvement was thus rapidly observed in 9 out of 10 patients treated with the combined therapy, while, in the other patient at stage C, subjective improvement could be documented. Although preliminary, this study indicates that a combined hormonal therapy which neutralizes all androgenic influences on peripheral tissues is of potential benefit in prostatic cancer. Moreover, the ease of application as well as the lack of secondary effects of the present approach should make possible its use early in the disease and should thus minimize the development of metastases and androgen-resistant cell clones. Randomized prospective studies on this potentially beneficial therapy are warranted.

Adenocarcinoma↗
PubMed1981

Additive inhibitory effects of treatment with an LHRH agonist and an antiandrogen on androgen-dependent tissues in the rat.

Combined treatment of adult male rats with the LHRH agonist, [D-Ser(TBU)6, des-Gly-NH2(10)]LHRH ethylamide, and a non-steroid antiandrogen, RU 23908, led to a rapid and marked atrophy of the ventral prostate and seminal vesicles. Treatment with the LHRH agonist decreased androgen secretion and thus facilitated the action of the antiandrogen in androgen-dependent tissues. Such a combined treatment could be useful in the treatment of androgen-dependent pathologies in man, particularly in prostatic adenocarcinoma and possibly benign prostatic hyperplasia.

Animals↗
PubMed1981

Parallel stimulation of ACTH, beta-LPH + beta-endorphin and alpha-MSH release by alpha-adrenergic agents in rat anterior pituitary cells in culture.

Characteristics of the alpha-adrenergic stimulation of ACTH, beta-endorphin + beta-LPH and alpha-MSH release were studied in rat anterior pituitary cells in primary culture. Parallel changes of ACTH, beta-endorphin + beta-LPH and alpha-MSh release were found under all stimulatory and inhibitory conditions by natural and synthetic catecholamine agonists and antagonists. (-)Epinephrine and (-)norepinephrine lead to a 8--10-fold stimulation of peptide release at ED50 values of 20 and 90 nM, respectively. The stereoselectivity of the alpha-adrenergic stimulatory action on peptide release is indicated by a 100-fold higher activity of (-)- than (+)norepinephrine while (-)epinephrine is 10 times more potent than the corresponding (+) stereoisomer. The involvement of a typical alpha-adrenergic mechanism in the control of release of ACTH, beta-endorphin and related peptides in rat anterior pituitary gland is indicated by the following order of potency of a series of catecholaminergic agents (ED50 values): (-)epinephrine (20 nM) greater than (-)norepinephrine (90 nm) greater than phenylephrine (400 nM) greater than isoproterenol (6000 nM). The stimulatory effect of (-)epinephrine or phenylephrine is completely reversed by low concentrations of the alpha-adrenergic antagonist phentolamine while the beta-adrenergic antagonist propranolol has no effect up to 10 muM. Beside providing an easily accessible pure population of post-synaptic alpha-adrenergic receptors having potential applications as a model for other less accessible alpha-adrenergic brain systems, the present data suggest the possibility of the direct involvement of a catecholamine in the physiological control of ACTH secretion in the rat anterior pituitary gland.

Adrenergic alpha-Agonists↗
PubMed1981

Sensitivity of rat adenohypophyseal cells to estradiol and LHRH during long-term culture.

To determine possible effects of the time in culture on the responsiveness of the different pituitary cell types to estrogens, rat anterior pituitary cells were incubated up to 20 days in the presence or absence of 10 nM 17 beta-estradiol. Whereas spontaneous luteinizing hormone (LH) and thyroid-stimulating hormone (TSH) release decreased by 85-90%, follicle-stimulating hormone (FSH) and prolactin accumulation in medium were only 50% decreased after 20 days in culture, thus suggesting that the secretion of FSH and prolactin is less dependent on extrinsic stimulatory factors. Estradiol increased spontaneous LH release and its responsiveness to luteinizing hormone-releasing hormone (LH-RH) up to day 16 in culture, whereas the stimulatory effect of the estrogen on FSH secretion was significant only up to day 6. The stimulatory effect of estradiol on basal TSH release was seen up to day 8 in culture, whereas that on spontaneous prolactin release increased progressively after day 8 in culture up to the last time interval studied (20 days). As revealed by immunocytochemistry, the stimulatory effect of estradiol was not due to changes of cell growth.

Animals↗
PubMed1981

Attempts to demonstrate peptide localization and secretion in primary cell cultures of fetal rat hypothalamus.

Primary cultures of dispersed hypothalamic cells were prepared from 18- to 19-day-old rat fetuses. Morphological studies revealed two types of cells having typical glial and neuronal appearances. Immunostaining of cells in culture was positive for neurophysin. The incubation medium contained radioimmunoassayable luteinizing hormone-releasing hormone, vasopressin, beta-endorphin and adrenocorticotropin hormone. The present data suggest that hypothalamic cells in primary culture secrete immunoreactive hormones or peptides; however, they do not seem to store significant amounts of these peptides.

Adrenocorticotropic Hormone↗
PubMed1981

Androgens decrease LHRH binding sites in rat anterior pituitary cells in culture.

[125I]-[D-Ser(TBU)6]LHRH-EA binds to a single class of high affinity sites in rat anterior pituitary cells in culture at an apparent dissociation constant of 0.25 nM at 0-4C. The order of potency of a representative group of LHRH agonists and antagonists to displace the labeled ligand is similar to their LH-releasing activity. Treatment of pituitary cells for 48 h with 100 nM 5 alpha-dihydrotestosterone leads to a 40% decrease of the number of LHRH receptors with no change of binding affinity. This loss of LHRH receptors is accompanied by a similar decrease of the LH responsiveness to LHRH, thus providing the first evidence for a direct effect of sex steroids on pituitary LHRH receptors as a possible mechanism of feedback action.

Androgens↗
PubMed1981

Interactions between 17 beta-estradiol and progesterone in the control of luteinizing hormone and follicle-stimulating hormone release in rat anterior pituitary cells in culture.

After preincubation of rat anterior pituitary cells in culture for 48 h with 10(-9) M 17 beta-estradiol (E2), basal LH release is increased 1- to 2-fold, while the concentration of LHRH required to induce a half-maximal stimulation (ED50) of LH release is approximately 50% reduced. The presence of 10(-7) M progesterone (P) alone for 48 h has no effect on LH release, but it inhibits the sensitizing action of E2 on the LH response to LHRH. This inhibitory effect of P on the E2-induced increase of LH responsiveness to LHRH is similar to the effect of androgens. While not affecting the LHRH ED50 for FSH release, P stimulates both basal FSH release and the maximal FSH response to LHRH. This effect of P is potentiated by simultaneous incubation in the presence of E2. The stimulatory effect of E2 alone on LH release is exerted at an ED50 value of 1-2 x 10(-11) M. A similar ED50 value is found for the potentiating effect of E2 on the P-induced stimulation of FSH release. The stimulatory effect of E2 on LH responsiveness to LHRH appears to be due to changes in the sensitivity of the release mechanisms in gonadotrophs, since the total hormone content (release plus cell content) is not affected by E2 under the same experimental conditions. The stimulatory effect of P on FSH release is measured at an ED50 value of 1 x 10(-8) M and is maximal after approximately 8 h of incubation with the steroid. While not affecting total LH, P increases total FSH (release plus cell content), indicating that the stimulatory effect of P on FSH release could be secondary to changes in the hormone content of cells.

Animals↗
PubMed1981

Dissociated changes of pituitary luteinizing hormone-releasing hormone (LHRH) receptors and responsiveness to the neurohormone induced by 17 beta-estradiol and LHRH in vivo in the rat.

A single injection of 17 beta-estradiol into castrated male or female rats results in an initial decrease in plasma concentrations of LH and pituitary responsiveness to LHRH, followed by a rapid return to normal or slightly elevated values. Under such experimental conditions, no acute change of binding of [125I-labeled D-Ser(TBU)6]LHRH ethylamide to anterior pituitary homogenate could be observed. Moreover, the self-priming effect of LHRH, as illustrated by a 10-fold increase in the LH response to a second injection of LHRH in the afternoon of proestrus, is accompanied by a 40% loss of pituitary LHRH receptors. During the estrous cycle, a 100% increase in pituitary LHRH receptors is already found on diestrus II, while the maximal LH responsiveness to LHRH occurs later, namely on the afternoon of proestrus. The present findings of a dissociation between changes in LHRH receptor levels and LH responsiveness to the neurohormone suggest that postreceptor events play a predominant role in the control of gonadotropin secretion by sex steroids and LHRH itself. Moreover, LHRH can cause an acute down-regulation of its own receptor in the anterior pituitary gland.

Animals↗