Biomedical subjects

W G Rossmanith

Publications and source records attributed to W G Rossmanith.

76 records · Page 5Linked to original sources

PubMed1988

Pulsatile beta-endorphin release from the human pituitary in vitro.

An in vitro perifusion system was used to characterize spontaneous immunoreactive beta-endorphin (i beta-END) release from 10 human fetal (20-23 weeks gestation) and 2 human adult anterior pituitaries. Spontaneous i beta-END release from fetal anterior pituitaries was pulsatile, with a mean (+/- SE) pulse interval of 9.1 +/- 0.5 minutes, pulse amplitude of 120.8 +/- 46.1 pg with nadir to peak increment of 106.0 +/- 32.9%, and overall release rate of 209.7 +/- 65.0 pg/2 minutes. Blockade of calcium activity with 10 microM verapamil and 4 mM EGTA suppressed the frequency and amplitude of the spontaneous pulsatile i beta-endorphin release (n = 2). Administration of 2 nM human CRF for 20 minutes at the end of 2 perfusions induced 205 and 883% increases of i beta-END release over the preceding basal levels. Administration of 2 nM CRF for 50 minutes at the end of another perifusion led to a greater and prolonged increase (maximum 4620% relative to the immediately preceding basal level) in i beta-END release. Addition of 56 mM KCl during the last 20 minutes of this prolonged CRF stimulation further increased i beta-END release (to 7680% relative to the baseline preceding the CRF stimulation). Each of 4 quarters of adult anterior pituitaries (2 quarters each from 1 male and 1 female) also released i beta-END in a pulsatile fashion, with a pulse interval of 11.8 +/- 2.0 minutes, pulse amplitude of 7.4 +/- 0.8 ng with nadir to peak increment of 51.4 +/- 15.3%, and overall release rate of 21.7 +/- 2.9 ng/2 minutes. These studies demonstrate that i beta-END release from the isolated human anterior pituitary in vitro is characterized by high-frequency pulses, independent of hypothalamic stimulation. This spontaneous calcium-dependent pulsatile i beta-END release apparently reflects the activity of an intrapituitary pulse-generating mechanism.

Adult↗

PubMed1987

Sleep-associated decrease in luteinizing hormone pulse frequency during the early follicular phase of the menstrual cycle: evidence for an opioidergic mechanism.

To investigate the possible role of an opioidergic mechanism(s) in the sleep-associated decrease in LH pulse frequency during the early follicular phase of the menstrual cycle, 10 normal cycling women were studied on days 3 and 4 of their cycles before and after the administration of a specific opiate receptor antagonist, naloxone. Sequential 24-h infusions of naloxone (10-mg iv bolus dose followed by an infusion of 30 micrograms/kg . h) or NaCl were administered randomly. Pulsatile LH activity was assessed for 48 h. Sleep was confirmed by electroencephalogram monitoring during the night hours (2300-0700 h). Significant sleep-associated decreases in LH pulse frequency (P less than 0.01) and mean serum LH levels (P less than 0.01) were found during the NaCl control studies. While naloxone infusion had no effect on LH pulse frequency during the waking hours, it prevented the sleep-associated decrease in pulse frequency and, in fact, significantly (P less than 0.001) increased the LH pulse frequency during the sleeping hours. These observations provide evidence that a diurnal variation of naloxone sensitivity exists in early follicular phase women and that the decrease in LH pulse frequency normally found during sleep is based at least in part on increased opioidergic inhibition.

Adult↗

PubMedDate not supplied

Gonadotropin secretion during aging in women: review article.

Biological aging during the postmenopause markedly affects the neuroendocrine control of gonadotropin release. The determination of the age-related dynamics on gonadotropin secretion in postmenopausal women have proven to be a valid approach for delineating changes as a function of progressive age. As a result, major functional derangements, primarily at a hypothalamic rather than a pituitary site, have been determined as concomitants of aging in women. Furthermore, aging may impair the negative feedback sensitivity to ovarian sex steroids, and interfere with the central neurotransmitter activity governing gonadotropin secretion. The data reviewed on gonadotropin secretion in postmenopausal women support the view that the age-related processes are related to a hypothalamic rather than to a pituitary hypofunction.

Activity Cycles↗

PubMedDate not supplied

Initial experiences with subcutaneous pulsatile human menopausal gonadotropin administration: successful induction of ovulation in patients with polycystic ovarian disease.

Human menopausal gonadotropin (hMG) was administered to 10 patients with polycystic ovarian disease (PCOD) who had failed to ovulate in response to clomiphene citrate. Five patients (group 1) were treated with intramuscular hMG injections daily, on an individually adjusted regimen. Five others (group 2) were stimulated with subcutaneous hMG in a pulsatile fashion by means of a portable infusion minipump. The pulse doses ranged between 3.5 and 7.7 IU FSH per pulse at a constant frequency of 90 minutes. Sixteen of 18 treatment cycles were ovulatory, 9 under intramuscular, and 7 under subcutaneous treatment. A total of two patients conceived with singleton pregnancies, one in each treatment group. Neither ovarian hyperstimulation nor complications of injections were noted. The amount of subcutaneous hMG required to achieve ovulation was significantly less (46.5%; P less than .001) than that needed with intramuscular administration. However, there were no differences in the duration of stimulation periods, the lengths of luteal phases, or serum E2 and gonadotropin levels between the groups. In conclusion, pulsatile subcutaneous hMG administration may be an alternative delivery mode for patients with PCOD.

Adult↗