Alcohol effects on HCG stimulated gonadal hormones in women.
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Adult↗
Biomedical subjects
A Skupny
Publications and source records attributed to A Skupny.
Alcohol effects on hCG-stimulated gonadal hormones in women.
Chronic alcohol abuse is associated with derangements of reproductive function in women. The mechanism of increased risk for alcohol-related abortions and fetal alcohol syndrome is unknown. The goal of this study was to determine if acute alcohol administration affected gonadal steroid hormone levels after administration of human chorionic gonadotropin (hCG) to normal healthy women. hCG was used to simulate the hormonal milieu during the first trimester of pregnancy. Ten women were studied during the mid-luteal phase (between days 17 and 23) of their menstrual cycle. Plasma estradiol, progesterone and prolactin were measured before and after simultaneous administration of 5000 I.U. of hCG (Profasi) and alcohol or placebo solution under double-blind conditions. There was a significant increase in plasma estradiol (P less than .001) and prolactin levels (P less than .01) after hCG and alcohol administration but not after hCG and placebo administration. Plasma progesterone increased significantly (P less than .001) above base line after hCG and placebo administration but this was not observed after hCG and alcohol administration. Since progesterone is essential for the maintenance of pregnancy, alcohol's attenuation of the expected progesterone response to hCG stimulation could increase the risk of spontaneous abortion. An alcohol-induced increase in estradiol after hCG administration could contribute to risk for fetal dysmorphology during the first trimester of pregnancy.
Administration, Oral↗
Acute alcohol effects on plasma estradiol levels in women.
Acute administration of alcohol (0.695 g/kg) to healthy adult women resulted in peak blood alcohol levels between 70 and 75 mg/dl within 50-60 min after initiation of drinking. Alcohol induced a significant increase (means = 18 pg/ml) in plasma estradiol levels (P less than 0.01). In contrast, after placebo ingestion, plasma estradiol levels did not change significantly. After alcohol intake, plasma estradiol levels reached peak values at 25 min following initiation of drinking when blood alcohol levels averaged 34 mg/ml. It is postulated that the alcohol-induced increase in plasma estradiol is due to changes in hepatic redox states associated with the catabolism of ethanol.
Adult↗
Naltrexone effects on pituitary and gonadal hormones in male and female rhesus monkeys.
The long-acting opioid antagonist, naltrexone, stimulates LH and FSH in women during the early follicular phase of the menstrual cycle and is a new provocative test of hypothalamic-pituitary function (42,63). The acute effects of naltrexone (0.25, 0.50 and 1.0 mg/kg IV) on anterior pituitary (LH, FSH, PRL) and gonadal steroid (T or E2) hormones were studied in 7 female and 4 male rhesus monkeys (Macaca mulatta). Integrated plasma samples were collected at 20 min intervals for 60 min before and for 300 min after intravenous infusion of naltrexone over 10 min. In females studied during the early follicular phase (cycle days 1-3), naltrexone did not stimulate LH and significantly suppressed E2 (p less than 0.0003-0.0001) and FSH (p less than 0.006-0.0001). Naltrexone (0.50 and 1.0 mg/kg) also did not stimulate LH release in late follicular phase females (cycle days 10-12) when estradiol levels were in the peri-ovulatory range. FSH and E2 were significantly suppressed (p less than 0.01-0.05) after 1.0 mg/kg naltrexone, but not after 0.5 mg/kg naltrexone. However, in males all doses of naltrexone significantly stimulated LH (p less than 0.003-0.0001) and T (p less than 0.001-0.0001) but not FSH. LH increased significantly above baseline within 20 to 40 min and T increased significantly within 60 min. These gender differences in naltrexone's effects on pituitary gonadotropins and gonadal steroid hormones were unanticipated. These data are not concordant with clinical studies which report significant naltrexone stimulation of LH in men and in women during the early follicular phase.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Anterior pituitary, adrenal, and gonadal hormones during cocaine withdrawal.
Plasma luteinizing hormone (LH), prolactin, testosterone, and cortisol levels were determined in 16 patients after hospital admission for cocaine abuse, during the course of 4 weeks of hospitalization, and before discharge. Hyperprolactinemia was found at admission (mean +/- SD, 27.5 +/- 10.2 ng/ml) and persisted until discharge (mean +/- SD, 28.7 +/- 10.8 ng/ml). Plasma LH, testosterone, and cortisol levels were within normal limits. These findings suggest that persistent elevation of plasma prolactin levels after cocaine withdrawal may reflect a chronic cocaine-induced derangement in neural dopaminergic regulatory systems.
Adult↗
Alcohol effects on naltrexone-induced stimulation of pituitary, adrenal, and gonadal hormones during the early follicular phase of the menstrual cycle.
Chronic alcohol abuse in women is associated with severe derangements of menstrual cycle regularity. However, acute alcohol ingestion has no effect on pituitary-gonadal secretory function. The purpose of this study was to determine whether acute alcohol ingestion altered the effects of naltrexone, a long-acting opioid antagonist, on pituitary, adrenal, and gonadal hormones in normal women. Fourteen women were studied during the early follicular phase (between days 2 and 4) of their menstrual cycle. Plasma LH, PRL, estradiol, progesterone, and cortisol concentrations were measured before and after administration of 50 mg naltrexone, orally, and alcohol or placebo solution given 1 h after naltrexone, under double blind conditions. Naltrexone significantly increased mean plasma LH (P = 0.02), PRL (P = 0.003), E2 (P less than 0.03), and cortisol (P less than 0.001) levels. Alcohol significantly augmented the naltrexone-stimulated increases in plasma LH (P = 0.006), estradiol (P less than 0.004), and cortisol (P less than 0.001) levels and significantly decreased plasma progesterone levels (P = 0.001). Plasma PRL increased (P = 0.001) to the same extent after naltrexone and alcohol ingestion or naltrexone and placebo. We conclude that alcohol enhances naltrexone-induced increases in plasma gonadotropins and adrenal and gonadal steroid hormones in women during the early follicular phase of the menstrual cycle.
Adrenal Cortex Hormones↗
Alcohol self-administration by female macaque monkeys: a model for study of alcohol dependence, hyperprolactinemia and amenorrhea.
Chronic alcohol dependence produces persistent amenorrhea in alcoholic women and female Macaque monkeys but the mechanism is unknown. In one amenorrheic alcohol-dependent monkey, prolactin levels increased from 16.5 to 63 ng/ml during chronic, high-dose alcohol self-administration (3.4 g/kg/day) and immunocytochemical examination of the anterior pituitary showed apparent hyperplasia of the lactotrophs. These data suggested that hyperprolactinemia might contribute to alcohol-induced amenorrhea. Four amenorrheic cycles (85-194 days) from two other alcoholic female monkeys that self-administered an average of 2.97 to 4.4 g/kg/day of alcohol were also studied. Each monkey became amenorrheic during the first menstrual cycle that alcohol was available. One monkey developed galactorrhea during a 97-day amenorrheic cycle when alcohol self-administration averaged 3.35 g/kg/day. Although prolactin levels were intermittently elevated above 20 ng/ml, average levels during these amenorrheic cycles (14.7 +/- 1.8 to 19.6 +/- 1.5 ng/ml) did not differ significantly from prolactin levels during normal ovulatory menstrual cycles when no alcohol was available (19.7 +/- 0.36 ng/ml). There was a negative correlation between daily alcohol dose and prolactin levels (p less than .01). High-dose alcohol self-administration was often associated with low normal prolactin levels, but a relative fall in alcohol dose was usually associated with elevated prolactin levels. These data suggest that both alcohol intoxication and relative alcohol withdrawal may alter basal prolactin levels. LH levels were significantly lower during amenorrheic cycles (16.9 +/- 1.2 to 24 +/- 1.4 ng/ml) than during nonalcohol control cycles (28 +/- 1.2 to 30 +/- 2.2 ng/ml) (p less than .001). These data are consistent with clinical data that suggest that hypothalamic amenorrhea is associated with suppression of gonadotropin secretory activity.
Alcohol Drinking↗
Alcohol effects on naloxone-stimulated luteinizing hormone, follicle-stimulating hormone and prolactin plasma levels in female rhesus monkeys.
Alcohol's effects on hypothalamic function were examined under conditions of opioid antagonist stimulation. The effects of naloxone (0.5 mg/kg i.v.) on anterior pituitary hormone plasma levels after alcohol (2.5 and 3.5 g/kg) or sucrose control administration were studied in 10 normal female monkeys (Macaca mulatta) during the luteal phase of the menstrual cycle. Naloxone was administered 60 or 90 min after nasogastric alcohol administration when blood alcohol levels were above 120 and 140 mg/dl. The rate of naloxone infusion (i.v. bolus or slowly over 10 min) and basal levels of progesterone were critical determinants of the anterior pituitary response to opioid antagonist stimulation. Bolus administration of naloxone did not stimulate luteinizing hormone (LH) or follicle-stimulating hormone (FSH) under control or alcohol conditions. Slow naloxone infusion significantly stimulated LH (P less than .01-.05), but not FSH, in monkeys with high basal progesterone levels (14.1-15.8 ng/ml) under both control and alcohol conditions. Naloxone stimulation of LH was equivalent under control and 2.5 g/kg alcohol conditions (60 and 53% above base line). The LH response to naloxone was enhanced after administration of 3.5 g/kg alcohol and increased to 151% above base line (P less than .01) in monkeys with high progesterone levels. In monkeys with low progesterone levels (3.6-4.6 ng/ml), slow naloxone infusion did not stimulate LH or FSH after sucrose control or 3.5 g/kg alcohol administration, but LH increased (P less than .05) after 2.5 g/kg alcohol administration. A slow infusion of naloxone suppressed PRL levels significantly below base line after sucrose and alcohol administration in monkeys with high (P less than .01-.0002) and low progesterone levels (P less than .0001). Naloxone suppression of PRL was equivalent after alcohol and sucrose control administration. Alcohol alone did not suppress PRL levels significantly. We conclude that acute alcohol administration, with peak blood alcohol levels above 240 and 300 mg/dl, does not attenuate hypothalamic and pituitary responsivity to naloxone stimulation.
Animals↗
Alcohol effects on LH and FSH in recently ovariectomized female monkeys.
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Animals↗
Hyperprolactinemia during cocaine withdrawal.
Plasma prolactin levels were determined for 8 patients (7 males and 1 female) who reported an average of 3.7 years of cocaine abuse. The mean prolactin level for these 8 patients 24 to 72 hours following admission to the hospital was 20.58 (S.E. +/- 3.2) ng/ml. Hyperprolactinemia (greater than 20 ng/ml) was detected in 4 patients and 3 others had high borderline prolactin levels. Only 1 patient had a normal prolactin value at the time of admission to the hospital. The mean prolactin level obtained prior to the patients' discharge from the hospital was 31.7 (S.E. +/- 5.3) ng/ml. Five of the 8 patients had an increase in prolactin levels between time of admission and discharge from the hospital. The mean increment in plasma prolactin levels for these 5 patients was 15.5 (S.E. +/- 4.2) ng/ml (P less than .02). Two patients who had significant hyperprolactinemia (greater than 50 ng/ml) at the time of discharge from the hospital reported self-administering the highest cocaine dose (6-8 gm per week) of the 8 patient cohort. Since cocaine blocks dopamine reuptake and prolactin secretion is regulated, in part, by dopaminergic inhibitory mechanisms, cocaine withdrawal may induce rebound supersensitivity of prolactin secretion. Findings obtained in this study suggest that cocaine-related derangements in prolactin secretion may be a biologic marker of a protracted cocaine abstinence syndrome.
Adult↗
Alcohol effects on naloxone-stimulated luteinizing hormone, prolactin and estradiol in women.
Plasma luteinizing hormone (LH), estradiol, prolactin and progesterone levels were measured in nine normal adult women prior to and following administration of naloxone and oral ingestion of ethanol or placebo-control solution. Each subject served as her own control in a double-blind study carried out during the midluteal phase of the menstrual cycle. The mean (+/- SD) progesterone level was 13.9 +/- 1.3 during control conditions and 13.9 +/- 1.7 during alcohol conditions. The mean peak blood alcohol level was 100 +/- 13 mg/dl within 45-60 min after initiation of drinking. Under placebo-control conditions, naloxone stimulated a significant increase in plasma LH and prolactin but did not increase estradiol or progesterone. Alcohol did not attenuate the significant naloxone stimulation of LH, and progesterone levels were equivalent under alcohol and control conditions. Alcohol significantly enhanced naloxone stimulation of prolactin and estradiol. Alcohol administration significantly augmented the naloxone-induced increase in plasma prolactin levels. After alcohol administration, naloxone also induced a significant increase in plasma estradiol levels, which was sustained throughout the 180-min sampling period. The mechanisms underlying alcohol's enhancement of naloxone-stimulated prolactin and estradiol remain to be determined. The alcohol-related increase in naloxone-stimulated prolactin secretion may reflect increased hypothalamic and/or pituitary sensitivity to alcohol following endogenous opioid blockade by naloxone or an effect of increased estrogen levels. The significant increase in plasma estradiol levels following concurrent naloxone and alcohol administration may occur as a consequence of alterations in steroid biotransformation associated with intrahepatic ethanol catabolism.
Adult↗
Use of naltrexone as a provocative test for hypothalamic-pituitary hormone function.
Naltrexone (50 mg) administration to normal adult women during the early follicular phase of the menstrual cycle (day 1 to day 4 following onset of menstruation) induced a significant elevation in plasma LH, prolactin, ACTH and cortisol levels. Orally administered naltrexone appears to be a safe and effective compound for assessing function of the hypothalamic-anterior pituitary axis in women.
Adrenocorticotropic Hormone↗
Alcohol effects on luteinizing hormone-releasing hormone stimulated luteinizing hormone and follicle-stimulating hormone in ovariectomized female rhesus monkeys.
The effects of acute alcohol administration on anterior pituitary function were studied in five ovariectomized female rhesus monkeys. Integrated plasma samples were collected for 80 min before and 120 min after nasogastric intubation of alcohol (2.5 or 3.5 g/kg) or isocaloric sucrose control solution. Then synthetic luteinizing hormone-releasing hormone (LHRH; 100 micrograms/i.v.) was administered and plasma samples were collected for an additional 180 min. After sucrose control administration, LHRH stimulated a significant increase in luteinizing hormone (LH) within 30 min (P less than .001) and follicle-stimulating hormone (FSH) within 60 min (P less than .01). After alcohol administration, LHRH stimulated LH and FSH also increased significantly (P less than .01) when blood alcohol levels averaged 242 (+/- 26) and 296 (+/- 20) mg/dl. Moreover, there was an alcohol dose-dependent increase in LHRH-stimulated LH (P less than .01, .001) in comparison to control conditions, even though prealcohol and presucrose LH levels were equivalent. LHRH-stimulated FSH was also higher after 3.5 g/kg of alcohol than after 2.5 g/kg of alcohol and sucrose control administration (P less than .001) but base-line FSH levels before 3.5 g/kg of alcohol were also higher than control (P less than .05) or 2.5 g/kg of alcohol (P less than .001). An alcohol related enhancement of LHRH-stimulated LH without concomitant suppression of FSH in ovariectomized females contrasts with data reported previously in normally cycling females studied under identical conditions. The absence of ovarian steroid and/or ovarian peptide negative feedback in ovariectomized females may have permitted the synergistic effect of alcohol and LHRH on LH.
Animals↗
Spectrofluorimetric assay of serum cystine aminopeptidase in normal and diabetic pregnancy compared with total oestrogen excretion.
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Adolescent↗
Alcohol effects on LH and FSH in ovariectomized female monkeys.
The acute effects of alcohol (2.5, 3.0, 3.5 g/kg) and sucrose control solution on basal levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) were compared in recently and chronically ovariectomized female rhesus monkeys. Integrated plasma samples were collected at 20 min intervals for 3 hr before and 6 hr after nasogastric intubation of alcohol or isocaloric sucrose control solution. Baseline levels of LH and FSH were significantly higher in recently than in chronically ovariectomized females (p less than 0.001). Baseline LH pulse frequency was also significantly higher (p less than 0.001) in the recently ovariectomized group than in the chronically ovariectomized group (0.704 +/- 0.03 vs. 0.379 +/- 0.10 pulses/hr). FSH pulse frequency was equivalent in both groups (0.444 +/- 0.06 to 0.360 +/- 0.06 pulses/hr). After 2.5 g/kg of alcohol, peak blood alcohol levels were 243 to 256 mg/dl and LH decreased significantly (p less than 0.01) in both groups. After 3.0 g/kg alcohol, peak blood alcohol levels were 237 to 289 mg/dl, and basal LH levels (p less than 0.05) and LH pulse frequency (p less than 0.05) decreased significantly only in the recently ovariectomized group. After 3.5 g/kg of alcohol, peak blood alcohol levels exceeded 320 mg/dl, and LH did not change significantly in either group. Administration of 3.5 g/kg alcohol was associated with increased LH pulse amplitude in some individuals. Since lower alcohol doses (2.5 and 3.0 g/kg) and sucrose control administration were followed by a significant decline in LH (p less than 0.05-0.01) and the highest alcohol dose (3.5 g/kg) was not, these data suggest the possible influence of nonspecific "stress" on modulation of LH secretory activity. FSH did not change after sucrose administration in recently ovariectomized monkeys, but was significantly suppressed after 2.5 and 3.5 g/kg alcohol (p less than 0.05). In the chronically ovariectomized monkeys, FSH decreased significantly after administration of sucrose and all alcohol doses. LH suppression was not consistently associated with changes in FSH in either group--a finding consonant with the hypothesis that LH and FSH may be controlled by different hypothalamic regulatory factors.
Animals↗