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Effects of intravenous cocaine and cigarette smoking on luteinizing hormone, testosterone, and prolactin in men

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AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
DOI: 10.1124/jpet.103.052928

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  1. NIDA NIH HHS [K05-DA00064, R01-DA15067, K05-DA00101, T32-DA07252, P01-DA14528] Funding Source: Medline

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Cocaine and nicotine have a number of similar behavioral and neurobiological effects. This study compared the acute effects of cocaine and cigarette smoking on luteinizing hormone (LH), testosterone (T), and prolactin. Twenty-four men who met American Psychiatric Association Diagnostic and Statistical Manual criteria for cocaine abuse or nicotine dependence were given intravenous cocaine (0.4 mg/kg) or placebo-cocaine, or smoked a low or high nicotine cigarette under controlled conditions. Placebo-cocaine or low nicotine cigarette smoking did not change LH, T, or prolactin. Peak plasma levels of 254 +/- 18 ng cocaine/ml and 22.6 +/- 3.4 ng nicotine/ml were measured at 8 and 14 min, respectively. LH increased significantly after both i.v. cocaine and high nicotine cigarette smoking ( P < 0.01). These LH increases were significantly correlated with increases in cocaine and nicotine plasma levels (P < 0.001 - 0.003), and high nicotine cigarette smoking stimulated significantly greater increases in LH release than i.v. cocaine ( P < 0.05). Testosterone levels did not change significantly after either cocaine or after high nicotine cigarette smoking. After i.v. cocaine, prolactin decreased significantly and remained below baseline levels throughout the sampling period ( P < 0.05 - 0.01). After high nicotine cigarette smoking, prolactin increased to hyperprolactinemic levels within 6 min and remained significantly above baseline levels for 42 min ( P < 0.05 - 0.03). The rapid increases in LH and reports of subjective high after both i.v. cocaine and high nicotine cigarette smoking illustrate the similarities between these drugs and suggest a possible contribution of LH to their abuse-related effects.

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