Blackwell's Five-Minute Veterinary Consult Clinical Companion. Группа авторов

       A white pearlescent powder in its purest form, usually present as a hydrochloride salt. The street drug typically looks like a fine, white, crystalline powder and often contains substances such as cornstarch, talcum powder, or flour as extenders. Occasionally other drugs such as caffeine, levamisole, fentanyl, aminorex, or amphetamines are mixed with the cocaine.

       “Crack” cocaine is the freebase form that has been precipitated into rocks that can be smoked.

       Schedule II drug used for local anesthesia, where vasoconstriction may be advantageous.

       Cocaine is a tropane alkaloid obtained from leaves of shrubs in the genus Erythroxylaceae, which are domesticated tropical plants native to the Amazon and the eastern slope of the Andes in Bolivia and Peru.

       Although the active ingredient, cocaine, was only isolated in 1859 by German chemist Albert Niemann, the coca leaves have been used for both medicinal and recreational purposes by the native populations in South American for thousands of years.

       Cocaine is the only naturally occurring local anesthetic. It is also one of the most abused drugs in the world.

       Because of its use as a recreational drug and its powder formulation, residues of cocaine are occasionally found in blood and urine samples collected from horses in drug and medication control programs.

       Prohibited substance under USEF, FEI, AQHA, and ARCI regulations.

       The pharmacodynamics of cocaine involve the complex relationships of multiple neurotransmitters.

       It directly prevents the re‐uptake of dopamine, serotonin, and norepinephrine into presynaptic neurons.

       Like other local anesthetics, it produces direct effects on cell membranes – cocaine blocks sodium channel activity and thus prevents the generation and conduction of nerve impulses in electrically active cells, such as myocardial and nerve cells.

       Cocaine has not been well studied in the horse. Based on the scientific literature examining the effects of cocaine in other species, however, in the horse one would expect it to be well absorbed when administered via mucous membranes (e.g. intranasally) or the GI tract.

       In humans, peak concentrations occur within 5–10 minutes of smoking and within 60 minutes of intranasal administration.

       Some cocaine is excreted unchanged in the urine, but the vast majority is metabolized to benzoylecgonine, ecgonine methyl ester, norcocaine and other metabolites.

       Although cocaine has a short elimination half‐life, the half‐lives of cocaine metabolites are substantially longer.

       The lethal dose for cocaine in horses has not been determined and there are no reports of acute toxicity in the scientific literature.

       In mice the LD50 is reported to be 96 mg/kg following oral administration.

       In humans, recreational cocaine abusers typically have peak serum concentrations between 0.5 and 5 μM, but lethal toxicity has been observed with serum concentrations of cocaine of 10 μM.

       Neurological – ataxia, disorientation, euphoria, agitation, anxiety, seizures.

       Cardiovascular – tachydysrhythmia, severe hypertension, acute coronary syndrome in humans, stroke.

       Musculoskeletal – hyperthermia, cocaine‐induced rhabdomyolysis.