Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0600142 (hot flushes)
 1,242 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the feasibility of administering the GnRH antagonist [(Ac-pClPhe1,pClPhe2,DTrp3,DArg6,DAla10) GnRH] intermittently to inhibit ovulation, this agent was given to normal ovulatory cynomolgus monkeys once weekly for 4 weeks. Ovulation was blocked in all females (eight of eight) throughout the 32 study weeks and resumed within 14.3 +/- 3.8 (+/- SEM) days in six of eight primates. Interestingly, mean tonic serum estradiol levels were not significantly reduced during treatment. Conversely, although midcycle levels of estradiol were not found, moderate estradiol levels occurred but they did not elicit preovulatory LH surges during the week after GnRH antagonist injection. In a second study directed at clarifying the mechanism(s) by which estrogen-induced LH surges were blocked, monkeys received GnRH antagonist in the early through the midfollicular phase of the menstrual cycle during which an estrogen (n = 3) or a GnRH (n = 4) challenge test was given on cycle day 6. Among monkeys receiving estradiol benzoate or a bolus dose of GnRH during the GnRH antagonist regimen, only those given GnRH (four of four monkeys) had increased LH secretion. These responses were similar to those of control monkeys (n = 3). Indeed, the pituitary was refractory (three of three monkeys) to estrogen-positive feedback for the LH surge. These findings indicate the potential utility of intermittent GnRH antagonist treatment to achieve contraception by ovulation inhibition, without creating a severely hypoestrogenic milieu attendant with the risks of negative sequelae effecting bone calcium loss, hot flushes, and atrophy of estrogen-dependent genital tissues.
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PMID:Ovulation inhibition by administration of weekly gonadotropin-releasing hormone antagonist. 308 71

An elevation of plasma immunoreactive neurotensin (iNT) was found during menopausal hot flashes. The flash-associated increases in iNT were concomitant with several physiological changes, including increased heart rate, finger blood flow, and finger temperature. Plasma iNT during hot flashes increased 245 +/- 65% (+/- SEM; n = 41), peaking 3.6 +/- 0.4 min after the onset of the hot flash. Immunochemical and chromatographic analyses indicated that the components of iNT elevated during a hot flash consisted primarily of C-terminal-related variants of NT, but not NT itself or any of its known metabolites. The three major substances identified using high pressure liquid chromatography and a C-terminal-directed RIA that appeared in women with hot flashes were also present in plasma of women without hot flashes and men. Since NT is a vasoactive and cardioactive peptide that can also affect temperature regulation, our results suggest the active involvement of these variants of NT in hot flashes.
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PMID:Changes in neurotensin-like immunoreactivity during menopausal hot flashes. 399 60

This study was designed to fully correlate the temporal relationship between augmented digital perfusion, (vasodilatation) and hot flushes, peripheral temperature, plasma luteinizing hormone, (LH) epinephrine and norepinephrine. Plasma samples were measured every 3 min for 2-4 h, in 5 symptomatic women before and after estrogen replacement and in 3 asymptomatic post-menopausal women. In all 5 symptomatic women the augmented digital perfusion occurred at a mean (+/- SEM) of 1.5 +/- 0.2 min before the initiation of the flush, at least 3 min before the initial rise in temperature and 9 min before the LH rise. There was a significant (P less than 0.05) rise in epinephrine but not norepinephrine at 3 and 6 min after the initiation of augmented digital perfusion. Although subjective improvement occurred in all 3 women receiving estrogen, all measured parameters disappeared in only 1 subject and the 2 others continued having augmented digital perfusion, flushes, and temperature vasomotor changes although the related LH increase was absent. Surprisingly, asymptomatic women who never received estrogens also demonstrated similar augmented digital perfusion and temperature changes, but failed to show the LH related rise, as observed in women with short-term estrogen treatment. In conclusion, these results demonstrate that augmented digital perfusion consistently precedes the hot flush, the rise in temperature and plasma LH in symptomatic post-menopausal women. The increase in epinephrine may be a homeostatic mechanism to compensate for the peripheral vasodilatation. The finding that augmented digital perfusion and temperature changes also occur in asymptomatic post-menopausal women indicates that objective changes are more specific and reliable indicators of vasomotor instability than the subjective sensation of hot flushes.
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PMID:The relation of physiological changes to subjective symptoms in postmenopausal women with and without hot flushes. 653 33