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Biomedical subjects

J Ellingboe

Publications and source records attributed to J Ellingboe.

At least 37 records · Page 2Linked to original sources
PubMed1988

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↗
PubMed1988

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↗
PubMed1988

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↗
PubMed1987

Acute ethanol administration enhances plasma testosterone levels following gonadotropin stimulation in men.

Plasma levels of LH, FSH, prolactin (PRL), and testosterone (T) were assessed in six normal men following administration of a pharmacologic dose of gonadotropin releasing hormone (GnRH) (500 micrograms iv over a one-min period) with concomitant oral administration of either ethanol (0.695 g/kg of body weight over a 15-min period) or ethanol placebo. Acute ethanol administration had no effect on the response of either LH or FSH to GnRH. PRL levels increased following GnRH and administration of both ethanol and ethanol placebo. Ethanol administration enhanced the T response to GnRH (p less than 0.001 vs placebo). During the placebo condition, T levels did not rise significantly until 100 min after GnRH administration, at which time the mean increment over baseline was 101 +/- 20 ng/dl (+/- SEM). In contrast, following ethanol intake, T levels were significantly elevated within 30 min after GnRH administration, at which time the mean increment over baseline was 187 +/- 42 ng/dl. The mean T increments were 304 +/- 62 and 472 +/- 77 ng/dl, respectively, 60 and 105 min following GnRH and ethanol administration. The increase in T levels following acute ethanol intake and concomitant gonadotropin stimulation is in contrast to the well-documented effect of chronic ethanol intake on suppression of testosterone synthesis by testicular Leydig cells.

Adult↗
PubMed1987

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↗
PubMed1987

Acute effects of ethanol on sex hormones in non-alcoholic men and women.

Chronic alcohol consumption has long been known to interfere with reproductive function and sexual behavior, but specific effects of acute alcohol ingestion on sex hormones have been studied only recently. An attempt is made in this review to summarize and explain conflicting results from studies of the acute effects of alcohol on the hypothalamic-pituitary-gonadal axis, with healthy non-alcoholic men and women as subjects. In men, moderate to high doses of ethanol have been reported to suppress plasma testosterone. Although some clinical studies have not supported this observation, considerable evidence documents direct alcohol inhibition of testosterone biosynthesis in the testis. After alcohol ingestion, plasma LH remains unchanged or increases, probably because of reduced androgen negative feedback. In analogous studies with women during the late follicular phase of the menstrual cycle, alcohol does not decrease plasma estradiol or alter LH levels. Furthermore, it has been reported that plasma levels of estradiol, progesterone and testosterone increase during alcohol treatment in the midluteal phase, while gonadotropins tend to decrease. Alcohol has no effect on LH secretion in post-menopausal women. Because reports on the acute effects of alcohol in men have not been consistent, it remains to be determined if acute alcohol effects in men and women are really different. In men, provocative tests of gonadotropin response to LHRH stimulation were normal during periods of intoxication and hangover, indicating that ethanol has no significant direct effect on LH secretion at the pituitary level. It seems more likely that alcohol changes plasma levels of sex steroids by altering hepatic, gonadal, and possibly adrenal metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Does ethanol inhibit LH secretion in the rat?

A prevailing view among those studying neuroendocrine effects of ethanol is that acute doses suppress luteinizing hormone releasing hormone (LHRH) secretion, and consequently inhibit luteinizing hormone (LH) release in the rat. This phenomenon has not been observed in primates, and has been thought to be a species difference. The experimental procedures, however, have involved ethanol administration by oral or intragastric (ig) routes in humans and monkeys, but intraperitoneal (ip) or carotid artery injection in rats. It has also been suggested that inhibition of LH secretion by ethanol in rats is mediated by endogenous opioid peptides (EOP), because the effect can be reversed by the opiate antagonist naloxone. An alternative explanation is that ip ethanol injection might stress rats sufficiently to activate hypothalamic-pituitary-adrenocortical (H-P-A) and EOP systems that are well known to inhibit hormonal activities of the hypothalamic-pituitary-gonadal (H-P-G) axis. Presented here are preliminary results from experiments with male rats. When ethanol is administered ig, under relatively stress-free conditions, it does not inhibit LH secretion in gonadally intact or castrated males. In contrast, ip injection of the same ethanol dose (2.0 g/kg body wt) causes pronounced inhibition of LH secretion and concomitant increases in plasma prolactin (PRL) and corticosterone--indicative of a stress response. Furthermore, when ip ethanol administration is preceded by intracerebroventricular (icv) injection of a corticotropin releasing factor (CRF) antagonist (alpha-helical ovine CRF residues 9 to 41), the effects of ethanol on LH and corticosterone are blocked. These results indicate that it may be stress, rather than ethanol per se, that inhibits LHRH and LH secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

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↗
PubMed1986

Marihuana smoking suppresses luteinizing hormone in women.

Smoking a single 1-g marihuana cigarette containing 1.8% delta 9-tetrahydrocannabinol induced a 30% suppression of plasma luteinizing hormone levels (P less than .02) in women during the luteal phase of the menstrual cycle. After marihuana placebo cigarette smoking, no luteinizing hormone suppression was observed in the same women under double-blind conditions. Marihuana may have adverse effects upon reproductive function during the luteal phase of the menstrual cycle as a consequence of gonadotropin inhibition.

Cannabis↗
PubMed1985

Acute effects of marihuana on luteinizing hormone in menopausal women.

Plasma luteinizing hormone (LH) levels were determined under double blind crossover conditions in 10 healthy menopausal adult females prior to and following smoking of a 1-g marihuana cigarette containing 1.83% delta 9-tetrahydrocannabinol (THC) and a 1-g marihuana placebo cigarette. A significant increase in pulse rate and levels of intoxication occurred after marihuana smoking but not after smoking placebo cigarettes. LH levels determined before administration of marihuana and placebo cigarettes were not significantly different and were within the range of normal values for healthy menopausal women. No significant differences were found between LH levels following marihuana and placebo smoking.

Cannabis↗
PubMed1985

Alcohol effects on plasma luteinizing hormone levels in menopausal women.

Plasma luteinizing hormone (LH) levels were determined in five healthy post-menopausal adult females prior to, during, and following a period of acute alcohol intoxication. LH levels were also determined in the same women following acute administration of a nonalcoholic beverage which had identical isocaloric value of alcohol. Plasma samples were collected at 30-minute intervals from an indwelling intravenous catheter from 120 minutes prior to alcohol or isocaloric beverage administration to 300 minutes following beverage intake. All women became moderately intoxicated after acute alcohol administration and developed peak blood alcohol levels of 94 mg per dl between 60 to 90 minutes following alcohol intake. LH levels determined before administration of alcohol or isocaloric beverage were not significantly different and were within the range of normal values for healthy, post-menopausal women. No significant differences were found between LH levels following alcohol administration when compared with LH values after isocaloric beverage. These data indicate that acute alcohol intake which produces blood alcohol levels slightly below usual legal limits of intoxication does not suppress LH in post-menopausal females. Since post-menopausal females do not have significant estradiol feedback control of LH secretory activity, and since LH secretory activity in post-menopausal women (in contrast to pre-menopausal females) is more sensitive to the inhibitory actions of drugs which may affect adrenergic and dopaminergic pathways in brain, the findings obtained in this study do not support an acute alcohol effect upon hypothalamic-pituitary modulation of gonadotrophin release in humans.

Ethanol↗
PubMed1985

Acute effects of marihuana smoking on prolactin levels in human females.

Plasma prolactin levels were determined in 16 healthy adult females before and after marihuana cigarette (1.83% delta 9-tetrahydrocannabinol) and placebo cigarette smoking. All subjects served as their own controls in double blind studies which were carried out on a residential research ward facility. Eight women were studied during the follicular phase and eight women were studied during the luteal phase of the menstrual cycle. Marihuana smoking did not produce any significant changes in plasma prolactin levels during the follicular phase of the menstrual cycle. However, plasma prolactin levels were significantly lower at 60 to 120 min (P less than .01) and 150 to 180 min (P less than .05) after marihuana smoking during the luteal phase of the menstrual cycle. Marihuana-induced suppression of plasma prolactin levels occurs in women but has not been observed in studies with human males.

Adult↗
PubMed1985

Alcohol effects on luteinizing hormone and testosterone in male macaque monkeys.

The effects of alcohol (2.5 and 3.5 g/kg) on luteinizing hormone (LH) and testosterone were studied in adult male macaque monkeys under both basal and naloxone-stimulated conditions. Integrated plasma samples were collected at 30-min intervals for 90 min before nasogastric intubation of alcohol (2.5 and 3.5 g/kg) or a sucrose control solution, isocalorically equivalent to 2.5 g/kg of alcohol. Under basal (non-naloxone-stimulated) conditions, alcohol (2.5 or 3.5 g/kg) did not change LH levels significantly from prealcohol control levels. When basal testosterone levels were normal (600-1300 ng/dl), alcohol significantly suppressed testosterone levels in a dose-dependent manner. Testosterone levels decreased by 52% (P less than .05) within 30 min after a 3.5 g/kg dose of alcohol. As average blood alcohol levels increased to 400 mg/dl and above, testosterone levels fell monotonically and remained over 70% below base-line levels (P less than .01). After administration of 2.5 g/kg alcohol, testosterone levels were significantly suppressed within 90 min (P less than .05) and remained 52 to 63% below control levels (P less than .02-.05) as average blood alcohol levels increased to 300 mg/dl. However, when basal testosterone levels were abnormally low (100-200 ng/dl), alcohol had no effect on testosterone or LH. Naloxone stimulation was used to circumvent the high incidence of abnormally low testosterone levels observed. Naloxone (0.5 mg/kg i.v.) administration 90 min after alcohol (2.5 and 3.5 g/kg) or sucrose control administration significantly increased LH levels in comparison to base line (P less than .02-.001). LH reached peak values within 60 min after naloxone administration. A significant increase in testosterone (P less than .001) was observed 90 min after naloxone administration as LH levels began to decline. Alcohol (2.5 and 3.5 g/kg) did not attenuate or delay naloxone-stimulated increases in LH and testosterone in comparison to sucrose control conditions.

Animals↗
PubMed1984

Perseveration of attention to conspecific odors and novel objects in castrated gerbils.

Castrated male and female gerbils were tested for odor preference and for attention to conspecific odors and a novel object. Castrated gerbils housed with sham-operates preferred home odors, discriminated between two groups of male gerbils by olfactory cues, and perseverated in attention to odors of male gerbils and to a novel object. Similar perseveration to male conspecific odors was shown in gerbils given injections of L-DOPA (30 mg/kg). Combined treatment (castration and L-DOPA) resulted in additive effects on perseveration. This research challenges two general hypotheses of gonadal hormone function. The first, that changes in odor preference after castration are due to a loss in testicular androgen, is insufficient, because (1) female as well as male gerbils showed similar perseveration to odors, (2) there was a significant correlation between LH and duration of investigation of male conspecific odors, and (3) L-DOPA, the dopamine precurser, also caused perseveration to conspecific odors. The second, that gonadal hormones are responsible for persistence of attention, cannot be broadly generalized, because castration with resultant elevation of LH and regression of ventral glands resulted in perseveration of attention in male and female gerbils.

Animals↗
PubMed1984

Acute effects of natural and synthetic cannabis compounds on prolactin levels in human males.

Plasma prolactin levels were determined in 23 adult males prior to and following administration of delta 9-tetrahydrocannabinol (THC) (17.5 mg orally), a synthetic cannabis compound, Nabilone (2 mg orally), a 1-g marihuana cigarette containing 1.83% THC, smoked under controlled conditions and placebo capsules and cigarettes for each of the active cannabis compounds. In order to control for possible influence of previous cannabis use history on prolactin response, three groups of subjects were studied--regular (daily) marihuana users, intermittent (weekly) marihuana users, and occasional (monthly) marihuana users. Each subject served as his own control for each drug condition. Double blind studies were conducted on a residential research ward. All baseline prolactin values were within the normal range for healthy adult males. There were no statistically significant differences in plasma prolactin levels among the three subject groups prior to administration of THC, Nabilone, marihuana or their respective placebos. There were no statistically significant changes in prolactin levels following TCH, Nabilone or marihuana smoking. Only placebo administration to regular and occasional marihuana users was followed by a significant increase in plasma prolactin levels. These findings indicate that acute administration of cannabis compounds, either orally or via smoking, does not significantly affect plasma prolactin levels in adult human males.

Adult↗
PubMed1984

Lack of acute alcohol effects on estradiol and luteinizing hormone in female macaque monkey.

The effects of alcohol (1.5, 2.5, 3.5 g/kg) on 17-beta estradiol and LH were evaluated in adult female Macaque monkeys. Integrated plasma samples were collected prior to and following nasogastric intubation of alcohol or isocaloric sucrose control solutions. Samples were collected at 30 minute intervals over 240 minutes. Each alcohol dose and control was studied at menstruation, the peri-ovulatory and mid-luteal periods and the premenstruum. After low, moderate and high doses of alcohol, blood alcohol levels (BAL) averaged 140, 260 and 344 mg/dl at the peak of the ascending BAL curve. Despite high blood alcohol levels, there was no evidence of alcohol dose-related suppression of LH or 17-beta estradiol at any phase of the menstrual cycle. These data are consistent with our findings in human females that acute alcohol intoxication did not suppress LH or estradiol. The apparent resiliency of human and Macaque females to acute alcohol effects on reproductive hormones contrasts sharply with data obtained in males that alcohol significantly suppresses testosterone in all species studied.

Animals↗