Cocaine is an alkaloid extracted from the leaf of the Erythroxylon coca bush. The hydrochloride salt is water soluble and can be administered orally, intravenously, or intranasally. The intravenous route of administration has an onset of action of 10-60 seconds, with a peak effect achieved in minutes and duration of effect that lasts up to 1 hour. Administration of the drug by the intranasal route has an onset of action of up to 5 minutes, with a peak effect achieved in approximately 20 minutes. The total duration of action by the intranasal route is 1 hour. The free-base form, known as crack cocaine, can be heated and smoked. This form has the quickest onset of action of 3-5 seconds, reaching its peak effect in 1 minute. (Lange and Hillis, 2001) The quick and intense effects of crack cocaine may potentially make it the most addictive form of the drug.
The effects of cocaine are mediated by blocking the synaptic reuptake of norepinephrine and dopa-mine, resulting in an excess of these neurotransmitters at the postsynaptic receptor. It is by this mechanism and the alteration of synaptic transmission that cocaine acts as a powerful sympathomimetic agent. Metabolism of cocaine occurs in the liver and its metabolites are detectable in blood or urine for up to 36 hours after administration. Cardiovascular complications of cocaine use include cerebrovascular accident (CVA), myocardial ischemia and infarct (MI), arrhythmia, and sudden death (McCann and Ricuarte, 2000). Intravenous administration of any substance of abuse increases the risk of the development of bacterial endocarditis. In contrast to the other drugs, endocarditis secondary to intravenous cocaine use more often affects the left-sided valves of the heart (Chambers et al., 1987).
Amphetamines produce many of the same effects as cocaine with similar routes of administration. In contrast to cocaine, amphetamines both stimulate the presynaptic release of dopamine and norepinephrine and then block their reuptake. High doses of amphetamine release 5-hydroxytryptamine (5-HT) and may affect serotonergic receptors. Metabolism occurs in the liver, mediated predominantly by the cy-tochrome P450 (CYP) 2D6 enzyme. As with cocaine, amphetamines are potent sympathomimetics and can cause MI, seizures, and CVA (Urbina and Jones, 2004).
Methamphetamine use has reached almost epidemic proportions among gay men in urban centers and is often associated with risk behaviors including sharing of needles for those who inject and unprotected sexual activity. Some have suggested that met-hamphetamines are associated with more intense sexual excitement. When amphetamines are taken along with sildenafil (Viagra), referred to as "sextasy," this combination allows for longer and rougher intercourse, which may promote tears in anal mucosa (Halkitis et al., 2001) and therefore promote HIV transmission. Compared to nonusers, gay men who use methamphetamine have been shown to have more sexual partners and to be more likely to participate in anal receptive intercourse, less likely to use condoms, and more likely to be HIV infected (Molitor et al., 1998; Shoptaw et al., 2002).
There is also a high prevalence of methamphet-amine use among predominantly heterosexual men and women in the West and Midwest. One study looking at risk behaviors in this population found that, compared to nonusers, the men who used metham-phetamine had more sex partners, had more vaginal and anal insertive intercourse, and were more likely to give or receive money or drugs in exchange for sex (Molitor et al., 1999). The investigators found that the women who used methamphetamine also reported more acts of vaginal intercourse that were not related to prostitution. Both men and women users were less likely to report always using a condom during sex than were nonusers; they were also more likely to use improperly cleaned, used needles and syringes (Molitor et al., 1999). These studies indicate that metham-phetamine users may represent a special subpopulation of both injecting and non-injecting drug users that are at particular risk for contracting and spreading HIV.
The mechanisms of action and toxicities for meth-amphetamine are the same as those for other amphetamines mentioned above. Chronic use leads to reduction of dopamine transporter levels and neuro-psychological impairment. Some investigators have suggested that methamphetamine use can enhance neurotoxicity in HIV patients and accelerate the development of HIV-associated dementia (Urbina and Jones, 2004).
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