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Biomedical subjects

R Soldani

Publications and source records attributed to R Soldani.

28 records · Page 2Linked to original sources

Lipid-independent therapeutic properties of transdermal 17 B-estradiol on cardiovascular diseases.

A low dose of transdermally administered 17 B-estradiol promptly improved a severe, treatment-unresponsive, cardiac arrhythmia initiated after the menopause in a woman with type-II familial hyperlipoproteinemia. The same treatment normalized the hypertension initiated after ovariectomy, in a woman who was only poorly controlled by anti-hypertensive drugs. These two cases are the first clear report of cardiovascular therapeutic properties of transdermal estradiol via mechanisms independent of lipoprotein modifications.

Administration, Cutaneous↗

Thermoregulatory and endocrine effects of a low dose of danazol in postmenopausal women: interaction with the effect of naloxone.

Before and on the 30th day of danazol administration (200 mg/day), in six postmenopausal women the activity of endogenous opioid peptides has been indirectly evaluated by the effect on LH secretion and body temperature (measured as rectal temperature) exerted by the infusion of the opioid antagonist naloxone (1.6 mg/h x 4 h preceded by 1.6 mg iv bolus). Before and during danazol administration a GnRH test (100 mcg iv bolus) was also performed to evaluate possible variations in pituitary responsiveness to GnRH. Danazol significantly reduced mean plasma levels of LH and FSH (p less than 0.01), and their response to GnRH stimulus (p less than 0.05). Either before or during danazol administration mean plasma LH and FSH levels did not vary during the infusion of naloxone, while body temperature significantly decreased (p less than 0.01). The decrease in body temperature was significantly greater (p less than 0.05) during danazol than before treatment. The present data suggest that in postmenopausal women a low dose of danazol exerts an antigonadotropic effect mainly reducing the pituitary responsiveness to GnRH. The enhanced hypothermic response to naloxone observed during danazol administration also seems to suggest that in postmenopausal women a low dose of danazol enhances the thermoregulatory role of endogenous opioid peptides.

Body Temperature Regulation↗

Neuroendocrine and clinical effects of transdermal 17 beta-estradiol in postmenopausal women.

The neuroendocrine and clinical effects of transdermal 17 beta-estradiol (rated at 50 micrograms/day; TTS 50) were studied in 40 postmenopausal women; ten additional postmenopausal women did not receive any drugs. The changes in LH and rectal temperature induced by the infusion of the opioid antagonist naloxone (10 mg i.v. bolus plus 10 mg/h for 4 h) were used to evaluate the central activity of endogenous opioid peptides. TTS 50 increased opioid activity, as evidenced by the restoration of the LH response (P less than 0.01) and the enhancement of the hypothermic effect (P less than 0.05) of naloxone. A greater reduction in hot flushes was observed in TTS 50-treated subjects than in untreated women, with the maximal effect of TTS 50 achieved after 3 months of therapy. TTS 50 did not modify the concentrations of circulating lipids, glucose or liver enzymes but reduced the biochemical parameters indicative of bone reabsorption. Bone density of the distal radius significantly increased during TTS 50 (P less than 0.02), reaching its maximum value after 6 months of therapy. Thereafter bone density declined, but more slowly than in untreated women. Our data suggest that TTS 50 has marked neuroendocrine effects, that it diminishes the incidence of hot flushes and reduces bone demineralization. By contrast, it has a very little, if any, metabolic impact on the liver or on glucose and lipid metabolism.

Administration, Cutaneous↗

Altered neuroendocrine regulation of luteinizing hormone secretion in postmenopausal women with Parkinson's disease.

The secretion of gonadotropins and the role exerted by the endogenous opioid system on luteinizing hormone (LH) secretion were investigated in 6 postmenopausal women affected by idiopathic Parkinson's disease (PD) as well as in 6 age- and weight-matched normal postmenopausal women as controls. The mean plasma follicle-stimulating hormone (FSH) and LH levels were evaluated both under basal conditions and after 20 days of conjugated estrogen administration (1.25 mg/day). At the same time, the activity of the endogenous opioid system was evaluated, as well as the LH response to the 4-hour infusion of the opioid antagonist naloxone (1.6 mg i.v. bolus followed by 1.6 mg/h). Both before and during estrogen administration, plasma FSH levels were similar in the two groups of subjects, whereas plasma LH levels were significantly lower (p less than 0.01) in parkinsonian than in control women. In each subject estrogen administration significantly blunted (p less than 0.01) plasma FSH levels. Plasma LH levels were reduced only in controls (p less than 0.05), but not in women with PD. In each subject, before estrogen administration, the plasma LH levels did not vary during naloxone infusion. In control women after 20 days of estrogen administration, the plasma LH levels significantly increased during naloxone infusion (p less than 0.01). By contrast, in women with PD, conjugated estrogens failed to restore the LH response to naloxone. The present results suggest that the neurotransmitter mechanisms, which regulate LH secretion, are altered, and, in particular, the activity of the endogenous opioid system is deficient in women with PD.

Aged↗

Effect of naloxone on body temperature in postmenopausal women with Parkinson's disease.

The role exerted by the endogenous opioid system on thermoregulation has been studied in six postmenopausal women affected by Parkinson's disease and in 6 age-matched, normal postmenopausal women, as controls. The women randomly received an infusion of the opioid antagonist naloxone (1.6 mg/h for 4 h) or of saline on two consecutive days. Body temperature, as evaluated by rectal temperature, was significantly lower (p less than 0.05) in Parkinsonian than in normal women, and it did not vary during saline infusion, in either groups. Naloxone infusion significantly reduced (p less than 0.01) body temperature in normal postmenopausal women, but it was unable to modify body temperature in women affected by Parkinson's disease. The low basal body temperature values and the inability of naloxone to exert a hypothermic effect in women suffering from Parkinson's disease seem to constitute further evidence for an impaired regulation of body temperature and impaired activity of the endogenous opioid system in this pathology.

Aged↗

Effects of transdermal 17 beta-estradiol treatment and naloxone infusion on gonadotropin response to gonadotropin-releasing hormone in postmenopausal women.

Estrogens exert both inhibitory and stimulatory effects on the secretion of GnRH and gonadotropins in women. The endogenous opioid peptides seem to mediate, at least in part, the inhibitory action exerted by estrogens on LH secretion. However, the mechanisms that mediate the stimulatory effect of estrogens on LH secretion are still unclear. The present study was performed to evaluate whether the endogenous opioid peptides could also participate in the stimulatory effect that estrogens exert on the gonadotropin response to GnRH. In postmenopausal women, a GnRH test was performed both under basal conditions and during the second month of treatment with transdermal 17 beta-estradiol (E2). In untreated postmenopausal women, two different doses of naloxone infusion failed to modify the LH and FSH responses to GnRH stimulation. During treatment with transdermal E2, the LH response to GnRH was significantly increased, while the FSH response was similar to that before treatment. Naloxone completely counteracted the enhanced LH response to GnRH observed during E2 treatment. On the other hand, naloxone did not significantly modify the FSH response to GnRH. The present results confirm that E2 exerts a sensitizing effect on the pituitary LH response to GnRH and suggest that the endogenous opioid system could be involved in this effect.

Endorphins↗

Effects of the antidopaminergic drug veralipride on LH and PRL secretion in postmenopausal women.

Patterns of LH and PRL secretion have been evaluated in 15 postmenopausal women before and after the chronic blockage of the D2 dopamine receptors with veralipride (100 mg twice daily, for 30 days). In addition, the possible influence of the antidopaminergic drug on the activity of the endogenous opioid system has been evaluated by the infusion of the opioid antagonist naloxone, performed before and during veralipride administration. Mean plasma LH levels were significantly blunted (p less than 0.05) and mean plasma PRL levels were significantly increased (p less than 0.001) by veralipride administration. The frequency of both LH and PRL secretory pulses was not modified, while the mean pulse amplitude of both hormones was significantly increased (p less than 0.05 for LH; p less than 0.001 for PRL) by veralipride administration. In untreated postmenopausal women naloxone infusion did not modify LH secretion. Following veralipride, the infusion of naloxone significantly increased (p less than 0.05) the mean plasma LH levels, had no influence on the frequency and significantly reduced (p less than 0.01) the amplitude of LH pulses, expressed as the percent increase from the nadir to the peak. Both before and after veralipride administration, naloxone failed to modify the pattern of PRL secretion. In untreated postmenopausal women, the percentage of concomitant PRL and LH pulses was significantly higher (p less than 0.001) during naloxone than during saline infusion, and this effect was amplified by veralipride administration (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Dopamine Antagonists↗

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↗

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↗

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↗