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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.