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Biomedical subjects

N K Mello

Publications and source records attributed to N K Mello.

At least 127 records · Page 7Linked to original sources
PubMed1989

Alcohol, marijuana, and mood states in young women.

Potential predictors of 8 Profile of Mood States (POMS) factor scores were examined for 30 young women (mean age = 26.4 years). Prospective data were obtained from diary questionnaires and POMS ratings submitted daily during 3 consecutive menstrual cycles. Behavioral and social variables (heavy versus light marijuana smoking, consumption of both marijuana and alcohol on a given day, stress, and sexual activity) were stronger mood factor predictors than temporal or biological variables (weekends or menstrual cycle phase). Heavy marijuana users consistently reported higher negative moods and lower positive moods than light marijuana users.

Adult↗
PubMed1989

Alcohol effects on luteinizing hormone releasing hormone-stimulated anterior pituitary and gonadal hormones in women.

Plasma luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin, estradiol (E2) and progesterone were measured in 24 normal, adult women before and after i.v. administration of 100 micrograms luteinizing hormone releasing hormone (LHRH; Factrel) and p.o. ingestion of an alcohol (0.694 g of alcohol per kg b.wt.) or placebo solution. Twelve subjects were studied during the early follicular phase of the menstrual cycle and 12 subjects were studied during the midluteal phase of the menstrual cycle. During each menstrual cycle phase, six subjects received placebo solution and six subjects received alcohol solution administered under double-blind conditions. Mean peak blood alcohol levels of 113 to 122 mg/dl were measured 45 to 60 min after initiation of alcohol intake. LHRH stimulated a significant increase in LH after both alcohol (P less than .0001) and placebo (P less than .0001) administration, and this LH increase was equivalent during the follicular and the luteal phases of the menstrual cycle. LHRH also stimulated a significant increase in FSH levels after both alcohol and placebo intake during the follicular and luteal phases of the menstrual cycle (P less than .0001). There were no significant differences in LHRH-stimulated FSH between the alcohol and placebo conditions. Plasma prolactin levels also increased significantly after LHRH administration during the follicular and luteal phases of the menstrual cycle (P less than .0001). There were no significant differences in prolactin response to LHRH administration between the alcohol or placebo conditions during the follicular and luteal phases of the menstrual cycle. Plasma E2 levels did not increase significantly after LHRH administration and placebo alcohol during the follicular phase of the menstrual cycle.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Effects of alcohol abuse on reproductive function in women.

Alcohol abuse and alcoholism are associated with disorders of reproductive function in both men and women. Amenorrhea, anovulation, and luteal phase dysfunction may occur in alcohol-dependent women and alcohol abusers. Yet there has been relatively little research on the consequences of alcohol abuse for female reproductive function. Recent clinical and survey studies of alcohol effects on pituitary gonadotropins and gonadal steroid hormones in women are reviewed. Experimental studies of the acute and chronic effects of alcohol on the hypothalamic-pituitary-gonadal axis in normal women and in animal models are also described. Recent studies of the acute effects of alcohol on opioid antagonist and synthetic LHRH-stimulated pituitary gonadotropins are summarized. Possible mechanisms underlying alcohol-induced disruptions of menstrual cycle regularity are discussed.

Alcoholism↗
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

Differential tolerance development to buprenorphine-, diprenorphine-, and heroin-induced disruption of food-maintained responding in macaque monkeys.

Single daily subcutaneous injections of buprenorphine (1.0 mg/kg), diprenorphine (1.0 mg/kg), or heroin (1.0 mg/kg) were given over 25 consecutive days to examine the degree and the rate of tolerance development to drug-induced suppression of food maintained responding. One gram food pellets were available on a second order schedule (FR 4 VR 16: S) during the 1-hr sessions three times a day. All drug and saline control injections were given at 10:00 a.m., 1 hr before a food session. During the first three days of treatment all three drugs produced marked suppression of food-maintained performance. Recovery from buprenorphine- and diprenorphine-induced suppression of food-maintained responding occurred within four and eight days, respectively. By the 25th day of buprenorphine and diprenorphine treatment, operant responding for food increased significantly above control levels (p less than 0.01). In contrast, the significant heroin-induced disruption of food-maintained responding (p less than 0.01) persisted throughout the 25-day treatment period. Saline substitution for all three drugs resulted in a gradual return to control levels of food pellets earned. Linear regression analysis of the linear portion of the time-effect curve revealed significant differences in both the rate and the degree of tolerance development to these three drugs. These differences in tolerance development may reflect pharmacokinetic differences between the relatively short-acting heroin and the longer-acting diprenorphine and buprenorphine.

Animals↗
PubMed1988

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↗
PubMed1988

Progressive ratio performance maintained by buprenorphine, heroin and methadone in Macaque monkeys.

The relative reinforcing efficacy of buprenorphine (0.01-0.10 mg/kg/inj.), heroin (0.01-0.10 mg/kg/inj.), methadone (0.03-0.25 mg/kg/inj.) and saline were compared in Macaque male monkeys using progressive ratio procedures. Responding for drugs and food (1 g banana pellet) was maintained on a second order FR 4 (VR 16:S) schedule of reinforcement that required an average of 64 responses for each injection or food pellet. After 40 sessions (10 days) of stable performance, the number of responses for each drug injection was systematically increased until monkeys reached a breakpoint defined by 2 consecutive days of no drug injections. Progressive ratio breakpoints for heroin at intermediate and high doses (0.05 and 0.10 mg/kg/inj.) were two to three times higher than for any other drug (P less than 0.05). Breakpoints for buprenophine (0.01-0.10 mg/kg/inj.) were higher than for a low dose of methadone (0.03 mg/kg/inj.) but were equivalent to an intermediate methadone dose (0.10 mg/kg/inj.). Breakpoints for both low (0.01 mg/kg/inj.) and high (0.10 mg/kg/inj.) buprenorphine doses were greater than for intermediate doses (0.03 and 0.05 mg/kg/inj.) but these differences were not statistically significant. Linear regression and area under the curve analyses were used to quantify the rate at which drug maintained responding decreased by 30% of control levels as response requirements were increased. Extrapolated breakpoints derived from linear regression analyses were significantly correlated (P less than 0.05-0.01) with actual breakpoints for buprenorphine, heroin and methadone. The concordance between 'extrapolated' and traditional breakpoint ranking of these drugs suggests that regression analysis techniques can be used to predict traditional breakpoints.

Animals↗
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↗