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Biomedical subjects

A Cagnacci

Publications and source records attributed to A Cagnacci.

84 records · Page 5Linked to original sources
PubMed1989

Regulation of body temperature in postmenopausal women: interactions between bromocriptine and the endogenous opioid system.

The role exerted by the endogenous opioid system on thermoregulation has been studied in nine postmenopausal women before and after the chronic administration of the dopamine agonist bromocriptine (5 mg/day). These women randomly received an infusion of the opioid antagonist naloxone (1.6 mg/h for 4 h) or saline on two consecutive days, before and after 30 days of bromocriptine administration. Body temperature as evaluated by rectal temperature, did not vary during saline infusion performed both before and after 30 days of bromocriptine administration. In untreated women naloxone infusion significantly reduced body core temperature. The hypothermic response to naloxone was significantly greater following chronic bromocriptine administration. These results indicate that bromocriptine seems to increase the activity of the endogenous opioid system on the mechanisms which regulate body temperature in postmenopausal women.

Body Temperature Regulation↗
PubMed1989

Influence of oestradiol and progesterone on pulsatile LH secretion in postmenopausal women.

Pulsatile LH secretion was studied in six healthy postmenopausal women. Blood samples were obtained every 10 min during an 8-h saline infusion performed before and during the administration of transdermal oestradiol alone (E2; 50 micrograms/day) and in combination with vaginal progesterone (P; 100 mg twice daily). Plasma E2 and P levels reached values similar to those found in the early follicular phase and in the luteal phase of the menstrual cycle, respectively. The mean plasma LH levels significantly decreased (P less than 0.01) during transdermal E2 with and without vaginal P. A significant increase in the frequency (P less than 0.025) and the amplitude (P less than 0.05) of LH pulses was observed during transdermal E2. The administration of vaginal P to oestrongenized women significantly blunted the frequency (P less than 0.05) and enhanced the amplitude (P less than 0.05) of LH pulses. In all experimental conditions, the mean plasma LH levels showed a positive linear correlation with the amplitude of LH pulses. The present results show that peripheral levels of E2, similar to those of the early follicular phase of the menstrual cycle, can influence the pulsatile pattern of LH secretion, enhancing the frequency and the amplitude of LH pulses. In oestrogenized patients, the increase of peripheral P plasma levels to postovulatory values restored a pulsatile pattern of LH secretion similar to that of the early luteal phase of menstrual cycle.

Administration, Cutaneous↗
PubMed1988

Interaction between veralipride and the endogenous opioid system in the regulation of body temperature in postmenopausal women.

The influence of endogenous opioid peptides on body thermoregulation has been studied in untreated postmenopausal women and in the same subjects after chronic administration of the antidopaminergic drug veralipride (200 mg/day for 20 days). Subjects randomly received an infusion of the opioid antagonist naloxone (1.6 mg/h for 4 h) or saline on two consecutive days, both before and after veralipride treatment. In untreated subjects body core temperature, as evaluated by rectal temperature, did not vary during saline infusion, whereas a significant decrease was observed during naloxone infusion. Chronic administration of veralipride significantly increased the hypothermic response to naloxone. Therefore, veralipride seems to increase the activity of endogenous opioid peptides on mechanisms which regulate body temperature in postmenopausal women.

Body Temperature↗
PubMed1988

Chronic bromocriptine administration restores luteinizing hormone response to naloxone in postmenopausal women.

To evaluate whether dopaminergic treatment may modify endogenous opioid activity at the hypothalamic-pituitary level, the effects of naloxone infusion (1.6 mg/h for 4 h) on luteinizing hormone (LH) secretion were studied in 5 postmenopausal women either before or after chronic administration of the dopaminergic drug bromocriptine (BCT; 5 mg/day for 30 days). BCT administration did not modify mean plasma LH levels. Before treatment naloxone infusion did not induce any significant modification of LH secretion. Conversely, after chronic BCT administration naloxone induced a significant (p less than 0.05) increase in plasma LH levels. The LH response to naloxone was significantly (p less than 0.001) higher than that observed before BCT. The present data show that chronic BCT administration restores the LH response to naloxone in postmenopausal women. Therefore, these results seem to demonstrate that BCT administration can enhance opioid activity, suggesting an involvement of the endogenous opioid system in dopaminergic modulation of gonadotropin release.

Bromocriptine↗
PubMed1988

Restoration of luteinizing hormone response to naloxone in postmenopausal women by chronic administration of the antidopaminergic drug veralipride.

To determine whether antidopaminergic drug administration may modify endogenous opioid activity at the hypothalamic-pituitary level, the effects of naloxone infusion (1.6 mg/h for 4 h) on LH secretion were studied in six postmenopausal women before and after administration of the potent antidopaminergic drug veralipride for 20 days. Before veralipride administration, the naloxone infusion did not alter LH secretion. Chronic administration of veralipride resulted in a significant (P less than 0.01) decline in plasma LH levels. In addition, the naloxone infusion induced a significant (P less than 0.05) increase in plasma LH levels, which reached values similar to those before veralipride administration. These results demonstrate that in postmenopausal women the antidopaminergic drug veralipride can restore, at least in part, the activity of the endogenous opioid system. These findings suggest that endogenous opioid peptides may mediate the inhibitory effect exerted by chronic antidopaminergic drug administration on LH secretion in humans.

Adult↗
PubMed1988

Effects of the dopamine antagonist veralipride on hot flushes and luteinizing hormone secretion in postmenopausal women.

The effects on hot flushes of the dopamine antagonist Veralipride versus placebo were investigated in a randomized double-blind study of postmenopausal healthy women (N = 20 in each group). Cutaneous temperature recording and plasma LH pulsatility were studied in eight patients from each group. Veralipride administration (100 mg/day for 30 days) induced a significant (P less than .01) reduction in vasomotor symptoms and was more effective (P less than .05) than placebo. Treatment was followed by the expected increase (P less than .001) in plasma prolactin levels and by a significant decrease (P less than .05) in mean plasma LH. A significant reduction (P less than .01) was observed in objectively recorded hot flushes after Veralipride treatment, whereas there was no significant change in the characteristics of LH pulsatility. Infusion of the opioid antagonist naloxone (N = 5) induced a significant (P less than .01) increase in LH secretion after Veralipride administration. These results suggest that the endogenous opioid system may mediate the endocrine and clinical effects of long-term Veralipride treatment.

Climacteric↗
PubMed1987

Pulsatile luteinizing hormone release in postmenopausal women: effect of chronic bromocriptine administration.

Pulsatile LH release was studied in 28 healthy postmenopausal women by obtaining blood samples every 5 min for 4 h either basally or after 30 days of bromocriptine (BCT; 3.75 mg/day; n = 14) or placebo (n = 14) administration. Basally, mean plasma LH levels were 46.3 +/- 3.5 (+/- SE) and 53.4 +/- 4.6 mIU/mL in the BCT and placebo groups, respectively. Mean LH pulse frequencies were 4.2 +/- 0.3 and 4.0 +/- 0.4 pulses/4 h, mean pulse amplitudes were 19.2 +/- 1.9 and 20.1 +/- 1.5 mIU/mL, and mean interpulse intervals were 54.3 +/- 3.1 and 54.6 +/- 3.2 min in the two groups, respectively. BCT administration induced no significant changes in mean plasma LH levels, but it significantly (P less than 0.01) decreased LH pulse frequency (1.7 +/- 0.3 pulses/4 h) and amplitude (12.7 +/- 0.8 mIU/mL) and significantly (P less than 0.01) increased mean interpulse interval (126.1 +/- 17.5 min). Placebo administration did not induce any significant changes in pulsatile LH release. These results demonstrate that in postmenopausal women LH secretion is circhoral, and BCT administration can blunt LH pulsatility, suggesting dopaminergic regulation of the GnRH-LH pulse generator.

Bromocriptine↗
PubMed1986

Effects of different dopamine agonists and antagonists on post-menopausal hot flushes.

The dopaminergic system seems to be involved in both pulsatile luteinizing hormone (LH) secretion and hot flushes in post-menopausal women. With the aim of further clarifying its role, the effectiveness of dopaminergic and antidopaminergic drugs in the treatment of hot flushes was studied. Self-assessed scores for vasomotor symptoms were evaluated in 5 groups of 15 patients treated for 20 days with one of the following agents: placebo; the dopamine receptor agonist, bromocriptine; the indirect dopaminergic agent, Liposom; the antidopaminergic drug, veralipride or the peripheral antidopaminergic agent, domperidone. All of these treatment regimens were effective in alleviating hot flushes, but the pharmacological agents proved to be more effective than the placebo. A direct dopaminergic action is hypothesized in the case of bromocriptine and Liposom, while the antidopaminergic drugs might act through different indirect mechanisms such as the short-loop feedback exerted by hyperprolactinaemia on tuberoinfundibular dopamine (TIDA) neurons with a secondary dopamine-like activity, or stimulation of the opioid system.

Bromocriptine↗
PubMed1985

Sex steroids modulate prolactin response to naloxone in postmenopausal women.

To evaluate whether ovarian steroids modify the prolactin (PRL) response to opioid receptor blockade, the effects of naloxone infusion (1.6 mg/h for 4 h) on PRL secretion were studied in 5 postmenopausal women. Naloxone infusion was performed in basal conditions and after chronic oral treatment with conjugated estrogens (CE) (1.25 mg/day, for 20 days) or CE plus medroxyprogesterone acetate (MPA) (10 mg/day, for 20 days). Under basal conditions, 17 beta-estradiol, estrone, gonadotropin, and PRL plasma levels were in the normal range for postmenopausal women, and naloxone failed to affect PRL secretion. Naloxone induced a significant PRL increase after CE treatment alone (p less than 0.001) or in combination with MPA (p less than 0.001). The increase was significantly higher (p less than 0.05) after CE + MPA treatment than after CE treatment alone. These data suggest that steroids modulate the stimulatory effect of naloxone on PRL secretion in postmenopausal women.

Endorphins↗
PubMedDate not supplied

Continuous combined hormone replacement therapy with oral 17beta-estradiol and norethisterone acetate improves homocysteine metabolism in postmenopausal women.

OBJECTIVE: To evaluate the effect of a continuous combined oral hormone replacement therapy (HRT) on basal and post-methionine load homocysteine levels in postmenopausal women. DESIGN: Twenty-two postmenopausal women (PMW) were randomly allocated to receive either continuous combined oral HRT (2 mg of estradiol plus 1 mg of norethisterone acetate; n = 11) or no treatment (controls, n = 11) for 6 months. A methionine oral load (0.1 g/kg body weight) was performed in each subject at time 0 and after 6 months. Serum homocysteine levels were measured by high-performance liquid chromatography in samples collected at time 0 and at 4, 8, and 24 h after the methionine load, while levels of vitamin B6 (by high-performance liquid chromatography) and B12 and folate (both by ELISA) were assayed in samples collected at time 0. RESULTS: Serum levels of glucose and body mass index increased in treated PMW, whereas folate decreased in controls. In treated PMW, basal homocysteine tended to decrease (10.6 +/- 3.3 micromol/L vs. 9.62 +/- 2.8 micromol/L, p = 0.062), whereas in controls it significantly increased (10.7 +/- 2.65 micromol/L vs. 12.17 +/- 3.89 micromol/L, p < 0.05). This increase was not significant after correction for vitamin status (p = 0.072). Homocysteine values 4 h (31.9 +/- 13.53 micromol/L vs. 39.83 +/- 22.53 micromol/L, p < 0.05) and 8 h (35.1 +/- 13.13 vs. 43.34 +/- 22.15 micromol/L) after methionine, and integrated homocysteine response to methionine (392.5 +/- 133.8 micromol/24 h vs. 458.8 +/- 104.8 micromol/24 h; p < 0.05), were significantly reduced in HRT-treated, but not in untreated, PMW. CONCLUSIONS: Continuous combined oral HRT with17beta-estradiol plus norethisterone acetate reduces homocysteine levels, mainly after a methionine load. This effect seems to be independent of vitamin status and may have positive implications for the prevention of cardiovascular diseases in PMW.

Administration, Oral↗
PubMedDate not supplied

Transdermal administration of estradiol and norethisterone: effect on the uterus and uterine arteries.

OBJECTIVE: To evaluate the short- and long-term effect on the uterus, endometrium, and vascular reactivity of uterine arteries of sequential transdermal estradiol (50 microg/day) and norethisterone (0.25 mg/day in the last 14 days of each cycle). DESIGN: An intravaginal ultrasound evaluation was performed in 48 postmenopausal women before and at the 3rd and 12th month of treatment, during the last 3 days of both estradiol alone and estradiol plus norethisterone. An endometrial biopsy was also performed before and at the end of treatment. In 11 participants, intravaginal ultrasound and endometrial biopsy were repeated after 48 months of treatment. RESULTS: Uterine volume (33.7 +/- 3.3 cm3 to 56.8 +/- 3.7 cm3; p = 0.001) and endometrial thickness (3.07 +/- 0.48 mm to 5.74 +/- 0.41 mm; p = 0.001) increased within 3 months, with no further increases. Thickness was similar in the estradiol and estradiol-norethisterone phase. Endometrial hyperplasia was found in one participant at 12 months of treatment. A significant decrease (p = 0.002) in the pulsatility index of uterine arteries was observed only during the estradiol phase. After 48 months of treatment, the pulsatility index of uterine arteries was lower than at baseline (2.78 +/- 0.24 vs. 2.23 +/- 0.33; p = 0.044) even when evaluated in the combined phase. CONCLUSIONS: The transdermal administration of sequential estradiol and norethisterone reduces uterine artery resistance and induces a self-limiting growth of the uterus and endometrium.

Administration, Cutaneous↗