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Biomedical subjects

G Fink

Publications and source records attributed to G Fink.

At least 235 records · Page 13Linked to original sources
PubMed1981

Effect of manipulating central catecholamines on puberty and the surge of luteinizing hormone and gonadotropin releasing hormone induced by pregnant mare serum gonadotropin in female rats.

We have investigated the effect of manipulating central catecholamines on the timing of puberty (as assessed by vaginal opening) in female rats and the surge of luteinizing hormone (LH) and gonadotropin releasing hormone (GnRH) induced by pregnant mare serum gonadotropin (PMSG) in immature female rats. Manipulation of the catecholamines was carried out with either 6-hydroxydopamine (6-OHDA) administered with or without either desipramine (DMI) or pargyline, or alpha-methyl-p-tyrosine (alpha-MPT). The neonatal administration of 6-OHDA delayed puberty, an effect which was potentiated by pretreatment with DMI and was associated with a reduction in the rate of body growth. Catecholamine fluorescence in animals aged 60--65 days that had been treated with DMI followed by 6-OHDA was diminished only in the caudatus--putamen; treatment with 6-OHDA alone resulted in diminished fluorescence in the hypothalamus and in the intermediate but not the external layer of the median eminence. The neonatal administration of alpha-MPT had no significant effect on either the growth rate or the timing of puberty. Regular oestrous cycle occurred after puberty in animals treated with either 6-OHDA or alpha-MPT. The PMSG-induced LH surge was significantly enhanced by 6-OHDA (administered i.v.) plus DMI, and reduced by 6-OHDA injected in to the lateral ventricle (v). The inhibitory effect of 6-OHDA (v) was reduced by DMI, but in animals given 6-OHDA (i.v.) after pargyline there was a marked reduction in the height of the LH surge. There was a good correlation between the changes in the concentrations of LH in peripheral plasma and the concentrations of GnRH in pituitary stalk plasma in that the PMSG-induced surge of GnRH was significantly increased by 6-OHDA (i.v.) plus DMI and reduced by 6-OHDA (v). In animals treated with 6-OHDA (i.v. plus DMI catecholamine fluorescence was reduced only in the external layer of the median eminence, while after 6-OHDA (v) plus DMI degeneration was seen in the medial forebrain bundle. These results demonstrate a marked difference between the long-term and acute effects of 6-OHDA on the gonadotropin control system. Neonatal treatment with 6-OHDA plus DMI significantly delays puberty and the rate of body growth, but does not affect cyclical gonadotropin release and has no persistent effect on the hypothalamic catecholaminergic systems. The acute administration of 6-OHDA, depending upon the route of administration and whether it is given after DMI, can either potentiate or inhibit the PMSG-induced surge of GnRH and consequently LH by mechanisms which involve destruction, respectively, of either dopaminergic terminals in the median eminence or catecholaminergic fibres in the dorsal hypothalamus.

Animals↗
PubMed1981

Comparison of steroid and LH-RH effects on the responsiveness of hemipituitary glands and dispersed pituitary cells.

We have carried out further in vitro studies on the priming effect of LH-RH and the effect of steroids on pituitary responsiveness to LH-RH. In hemipituitary glands, the priming effect could be elicited only once within an 11-h period and was found to diminish significantly with time after the first exposure to LH-RH. Incubation with oestradiol-17 beta (E2) had no significant effect on the responsiveness of hemipituitary glands to LH-RH. By contrast, E2 increased the responsiveness of dispersed cell system. The presence of hypothalamus or synthetic LH-RH did not facilitate the effects of E2. Testosterone significantly reduced the spontaneous and LH-RH-induced release of LH while progesterone had no effect. Exposure to E2 alone in either of the systems did not produce a consistent increase in the total amount of LH in the system. Synthesis of LH was, however, stimulated by exposure to LH-RH for 48 h but not 12 h. These results demonstrate that there is a marked difference between the mechanisms by which LH-RH and steroids affect the responsiveness of the anterior pituitary gland to LH-RH.

Animals↗
PubMed1981

Pulmonary function abnormalities in Sjögren's syndrome and the sicca complex.

The frequency of pulmonary involvement in a group of 20 patients with Sjögren's syndrome or the sicca complex was evaluated with pulmonary function studies. In 12 patients pulmonary functional abnormalities were demonstrated. The most common abnormality was airway obstruction. Nine out of 13 patients with the limited variant of the disease (sicca complex) and three out of seven patients with the complete syndrome had abnormal pulmonary function.

Adult↗
PubMed1981

Effects of short-term constant light on the proestrous luteinizing hormone surge and pituitary responsiveness in the female rat.

We have investigated the effects of exposure to short-term constant light (LL) on the spontaneous, proestrous luteinizing hormone (LH) surge in the female rat. Exposure to LL during the 3 days preceding proestrus delayed and reduced the magnitude of the LH surge which was measured in blood samples taken from conscious animals through an intra-atrial catheter that had been implanted early on the morning of proestrus. The pituitary responsiveness to synthetic luteinizing hormone-releasing hormone (LHRH) in animals exposed to LL was reduced about 6-fold about the time of the LH surge compared with that in animals on a 14 h light- 10 h dark (LD) regimen. In contrast to animals on LD, treatment of rats on LL with estrogen and progesterone after ovariectomy failed to restore to normal the pituitary responsiveness which is markedly reduced by ovariectomy. The implantation of a silicone-elastomer capsule containing 17 beta-estradiol into rats on LL after ovariectomy did not facilitate pituitary responsiveness. These results suggest that exposure of the female rats to LL for 3 days causes a shift in phase of the LH surge (which may represent a free-running LH rhythm) and reduces the magnitude of the LH surge by a mechanism which may involve a reduction in the sensitivity to estrogen of the centres involved in LHRH release.

Animals↗
PubMed1981

Oestradiol-17 beta increases pituitary responsiveness by a mechanism that involves the release and the priming effect of luteinizing hormone releasing factor.

We have investigated the mechanism by which oestradiol-17 beta augments pituitary responsiveness to luteinizing hormone releasing factor (LH-RF). Adult rats were ovariectomized on the morning of dioestrus and implanted with either an empty silicone elastomer capsule or a capsule containing oestradiol-17 beta. Twelve hours later the LH response, tested by injecting 50 ng LH-RF/100 g i.v., was significantly greater in animals implanted with an oestradiol capsule compared with that in animals implanted with an empty capsule. The effect of oestradiol was blocked by sodium pentobarbitone administered 4 h before the test, and this block was overcome by infusing LH-RF during the 4 h period at doses which by themselves were not sufficient to evoke a large release of LH. We also measured LH-RF in pituitary stalk blood collected under Althesin anaesthesia between 4-6 and 12-13 h after ovariectomy and capsule implantation. The concentration of LH-RF in stalk plasma fell between these two collection periods in animals implanted with empty but not with oestradiol-filled capsules. The concentrations of LH-RF in stalk plasma, although relatively low, were significantly higher in animals bearing an oestradiol-containing capsule than the concentrations in peripheral plasma from similarly treated animals, and, by comparison with the LH-RF concentrations in peripheral plasma from animals infused with LH-RF, were sufficiently high to increase significantly the responsiveness of the pituitary gland. These data show that as well as acting directly on the pituitary gonadotrophs, oestradiol-17 beta increases the responsiveness of the anterior pituitary gland by a mechanism that involves the release and the priming effect of LH-RF.

Animals↗
PubMed1981

Changes in responsiveness of dispersed pituitary cells to luteinizing hormone releasing hormone at different times of the oestrous cycle of the rat.

Dispersed pituitary cells obtained from female rats with regular oestrous cycles were suspended in Bio-Gel columns and perfused with pulses of luteinizing hormone releasing hormone (LH-RH). There was a close relationship between the amount of LH released and the concentration of LH-RH in the perfusate. It was not possible to elicit the priming effect of LH-RH, but the LH-response changed markedly during the oestrous cycle in a manner similar to that seen in vivo; i.e. the responses of cells prepared from rats killed at pro-oestrus were much greater than the responses of cells prepared from rats killed on other days of the cycle. A similar change in responsiveness was obtained when the columns were perfused with 60 mmol K+/1, suggesting that at least part of the increase in pituitary responsiveness that occurs at pro-oestrus is not dependent upon changes in specific receptors for LH-RH.

Animals↗
PubMed1981

Constant light blocks diurnal but not pulsatile release of luteinizing hormone in the ovariectomized rat.

We have investigated the effects of constant light on the patterns of LH release in long-term ovariectomized rats. Some animals were implanted with a silicone elastomer capsule containing oestradiol-17 beta. Plasma samples in anaesthetized animals were taken from the external jugular vein and in conscious animals from an indwelling intra-atrial catheter. The pulsatile release of LH that occurred in animals not treated with oestrogen was unaffected by constant light or the steroid anaesthetic alphaxalone plus alphadolone acetate (Althesin), but was abolished by sodium pentobarbitone. However, the diurnal release of LH produced by increasing the concentrations of plasma oestradiol in conscious animals was blocked by constant light. Thus, these two rhythms of LH release are controlled by different neural pathways; the one concerned with diurnal LH release being suppressed by exposure to constant light.

Alfaxalone Alfadolone Mixture↗
PubMed1981

Ontogeny of the sensitizing effect of oestradiol and luteinizing hormone releasing hormone on the anterior pituitary gland of the female rat.

The ontogeny of the facilitatory effect of oestradiol and luteinizing hormone releasing hormone (LH-RH) on the responsiveness of the anterior pituitary gland to LH-RH has been studied in vitro using pituitary glands from female rats age 15, 17, 20, 31, 35 and 38 days. The facilitatory effect of oestradiol was already well established by day 15, while the facilitatory effect of LH-RH (priming effect) developed only after day 17. Although it increased the overall response of the gland to LH-RH, oestradiol did not selectively enhance the priming effect of LH-RH. Both the effect of oestradiol and LH-RH reached a peak on day 25, 7 days before vaginal opening in this colony, and, as assessed by measuring pituitary LH contents, were not dependent upon the synthesis of LH. These data show that different mechanisms may be involved in the facilitation of pituitary responsiveness by oestradiol and LH-RH, but that both mechanisms appear to depend more upon an increase in the sensitivity of the receptor/release apparatus rather than in the gonadotrophin content of the gonadotrophs.

Animals↗
PubMed1980

Gonadotrophin release in hypogonadal and normal mice after electrical stimulation of the median eminence or injection of luteinizing hormone releasing hormone.

Electrical stimulation of the median eminence, using parameters known to cause the release of LH in normal male mice, failed to elicit any gonadotrophin response in nypogonadal (hpg) male mice. Administration of 40 ng synthetic LH releasing hormone (LH-RH) resulted in release of LH from the pituitary gland of hpg mice, although the response was significantly lower than that of normal mice. These results were consistent with the hypothesis that the hypogonadal state of the hpg mouse results from a functional basence of LH-RH in the hypothalamus rather than from a lack of response of the pituitary gland to the releasing hormone.

Animals↗
PubMed1980

Luteinizing hormone releasing factor in pituitary stalk plasma from long-term ovariectomized rats: effects of steroids.

The concentration of LH releasing factor (LH-RF) was measured by radioimmunoassay in blood collected from the cut pituitary stalk of long-term ovariectomized rats anaesthetized with Althesin. Stalk plasma LH-RF concentrations were increased immediately after ovariectomy (carried out at oestrus) and low at 2 and 4 days after operation. The concentrations then began to increase to reach a level at 24-28 days which was significantly higher than the concentrations during the oestrous cycle except for the time of the ovulatory surge at pro-oestrus. This pattern was similar to that of the concentrations of LH in jugular venous plasma taken from the same animals before exposure of the pituitary stalk. Like peripheral plasma LH concentrations, the concentrations of LH-RF in stalk plasma fluctuated and fell significantly and rapidly after the intravenous injection of 1 microgram oestradiol-17 beta. The release of LH-RF in long-term ovariectomized rats, into which had been implanted an oestradiol-containing Silastic capsule, was similar to the diurnal pattern of LH release; the afternoon increase in stalk plasma LH-RF concentration could be blocked by sodium pentobarbitone administered at 13.00 h and augmented by administering this anaesthetic at 13.00 h of the preceding day. The stalk plasma LH-RF concentrations in animals injected with oestradiol benzoate (OB) followed 72 h later with either OB or progesterone were lower than the concentrations in animals injected only with oil. These data show that in the rat (1) ovarian steroids could moderate LH release ('negative feedback') by inhibiting LH-RF release, and that in long-term ovariectomized animals (2) the oestradiol-induced circadian pattern of LH release is due to a circadian pattern of LH-RF release, and (3) the surge of LH produced by administering OB followed by either OB or progesterone is probably due mainly to a massive increase in the responsiveness of the anterior pituitary gland to LH-RF.

Animals↗