Cocaine is a powerful stimulant of the sympathetic nervous system by inhibiting catecholamine reuptake, stimulating central
sympathetic outflow, and increasing the sensitivity of adrenergic nerve endings to norepinephrine (NE). It is known, from numerous studies,
that cocaine causes irreversible structural changes on the brain, heart, lung and other organs such as liver and kidney and there are
many mechanisms involved in the genesis of these damages. Some effects are determined by the overstimulation of the adrenergic system.
Most of the direct toxic effects are mediated by oxidative stress and by mitochondrial dysfunction produced during the metabolism
of noradrenaline or during the metabolism of norcocaina, as in cocaine-induced hepathotoxicity. Cocaine is responsible for the coronary
arteries vasoconstriction, atherosclerotic phenomena and thrombus formation. In this way, cocaine favors the myocardial infarction.
While the arrhythmogenic effect of cocaine is mediated by the action on potassium channel (blocking), calcium channels (enhances the
function) and inhibiting the flow of sodium during depolarization. Moreover chronic cocaine use is associated with myocarditis, ventricular
hypertrophy, dilated cardiomyopathy and heart failure. A variety of respiratory problems temporally associated with crack inhalation
have been reported. Cocaine may cause changes in the respiratory tract as a result of its pharmacologic effects exerted either locally or
systemically, its method of administration (smoking, sniffing, injecting), or its alteration of central nervous system neuroregulation of
pulmonary function. Renal failure resulting from cocaine abuse has been also well documented. A lot of studies demonstrated a high incidence
of congenital cardiovascular and brain malformations in offspring born to mothers with a history of cocaine abuse.
Keywords: Cocaine toxicity, cardiovascular toxicity, cocaine induced hepatotoxicity, prenatal exposure, pulmonary toxicity, cocaine-related renal injury, local and systemic effects, stress oxidative, norcocaina
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Published on: 14 November, 2012
Page: [5624 - 5646]