Cocaine is a stimulant of the central nervous system, with a local anesthetic action and powerful vasoconstrictive proprieties. It can be taken through nasal inhalation, parenteral administration (intravenous, sub-cutaneous, intra-muscular), orally, as smoke or through the rectum or the genital organs.

Cocaine, like all the other abusive stimulants, determines an alteration of the metabolism of the catecolamine. Unlike heroin addiction, where many of the medical complications of abuse are secondary to infections or to the presence of contaminants, many of the complications caused by cocaine are determined by the substance itself. Once in the blood circle, the catecolamine acts like circulating hormones and no longer as a neurotransmitter. As a consequence of the release of catecolamine, cocaine quickens cardiac frequency, heightens blood pressure and determines cutaneous vasoconstriction. As a result of the activation of the simpaticomimetic system we observe pupil dilation, dryness of the mouth and lack of appetite.

The most common effects are an uplifted mood and euphoric condition, a sense of increased energy and self-esteem, of mental lucidity, libido and muscular strength. Appetite and the need to sleep decrease sharply. In some cases a marked restlessness may be observed, with tremors and extreme talkativeness. These initial “positive” effects tend to push the consumer to repeat the assumption. The euphoric condition later gives way to a state of sickness, depression and restlessness.

In short, the action of cocaine consequently results in the release of dopamine in the synaptic space, together with norepinephrine, epinephrine and serotonin which all determine a prolonged and amplified effect. The adrenergic stimulation produces tachycardia, sweating, tremors and midriasis, while the increase of adrenergic tone is greatly responsible for vasospasms which determine hypertensive crises and myocardiac or intestinal ischemy, etc. The dopaminergic action contributes to this peripheric effect, but is mostly responsible for the effects on moods, whereas the serotoninergic action may determine hallucinations, hyperthermia, convulsive episodes and contribute to vasospasms.

After repeated dosages of cocaine, the phenomenon of tolerance begins, and the same dosage of the substance produces decreasing effects; the dosage is therefore progressively increased to obtain the same initial effect. Tolerance is the result of cellular adaptation and diminished biologic response. The phenomenon is especially visible in the euphoric effects, which explains why many increase the dosage and the frequency of assumption, reaching the so-called cocaine binge. On the other hand, tolerance of the cardiovascular effects of the substance resulted to be only partial; this “dissociation” in the development of tolerance to the central effects and the consequences on the cardiovascular apparatus may explain the toxic proprieties of cocaine and the deaths it provokes.

Excerpt from: Braglia D, Gerra G, Mezzelani P, Quaglio GL. Cocaina: farmacocinetica, abuso, dipendenza, detossificazione e trattamento. In: Trattamento completo degli abusi e delle dipendenze. Padova: Piccin, 2002.