Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Cocaine pharmacokinetics

C. Pharmacokinetics. Cocaine Is well absorbed from all routes, and toxicity has been described after mucosal application as a local anesthetic. Smoking and intravenous Injection produce maximum effects within 1-2 minutes, while oral or mucosal absorption may take up to 20-30 minutes. Once absorbed, cocaine is eliminated by metabolism and hydrolysis with a half-life of about 60 minutes. In the presence of ethanol, cocaine Is transesterified to cocaethyl-ene, which has similar pharmacologic effects and a longer half-life than cocaine. (See also Table 11-59.)... [Pg.171]

Cheng-Prasoff relationship, 65-66, 214 Cholecystokinin receptor antagonists, 80 Cimetidine, 9-10 Clark, Alfred J., 3, 3f, 12, 41 Clark plot, 114 Clearance, 165—166 Clinical pharmacokinetics, 165 Cocaine, 149, 150f Competitive antagonism description of, 114 Gaddum equation for, 101-102, 113,... [Pg.294]

Toluene, volatile nitrites, and anesthetics, like other substances of abuse such as cocaine, nicotine, and heroin, are characterized by rapid absorption, rapid entry into the brain, high bioavailability, a short half-life, and a rapid rate of metabolism and clearance (Gerasimov et al. 2002 Pontieri et al. 1996, 1998). Because these pharmacokinetic parameters are associated with the ability of addictive substances to induce positive reinforcing effects, it appears that the pharmacokinetic features of inhalants contribute to their high abuse liability among susceptible individuals. [Pg.276]

The importance of pharmacokinetics should not be underestimated. The effects of psychoactive drugs are determined not only by their pharmacodynamic mechanisms, but also by how much of the drug reaches the brain, and how fast it does so. A cardinal example of this involves the behavioral differences between chewing coca leaves, snorting cocaine... [Pg.67]

Sun L, Hall G, Lau CE. 2000. High-performance liquid chromatographic determination of cocaine and its metabolites in serum microsamples with fluorimetric detection and its application to pharmacokinetics in rats. J Chromatogr B Biomed Sci Appl 745(2) 315-323. [Pg.40]

Byrd GD, Davis RA, Caldwell WS, Robinson JH, deBethizy JD (1998) A further study of FTC yield and nicotine absorption in smokers. Psychopharmacology 139 291-299 Chaudhri N, Caggiula AR, Donny EC, Palmatier MI, Liu X, Sved AF (2006) Complex interactions between nicotine and nonpharmacological stimuli reveal multiple roles for nicotine in reinforcement. Psychopharmacology 184 353-366 Cone EJ (1995) Pharmacokinetics and pharmacodynamics of cocaine, J Analy Toxicol 19 459 78 Desai RI, Terry P (2003) Evidence of cross-tolerance between behavioural effects of nicotine and cocaine in mice. Psychopharmacology 166 111-119 Desai RI, Barber DJ, Terry P (1999) Asymmetric generalization between the discriminative stimulus effects of nicotine and cocaine, Behav Pharmacol 10 647-656... [Pg.396]

Cone EJ (1995) Pharmacokinetics and pharmacodynamics of cocaine, J Anal Toxicol 19 459-78 Cryan JF, Bruijnzeel AW, Skjei KL, Markou A (2003) Bupropion enhances brain reward function and reverses the affective and somatic aspects of nicotine withdrawal in the rat. Psychopharmacology 168 347-358... [Pg.505]

The local anesthetics can be broadly categorized on the basis of the chemical nature of the linkage contained within the intermediate alkyl chain group. The amide local anesthetics include lidocaine (7.5), mepivacaine (7.6), bupivacaine (7.7), etidocaine (7.8), prilocaine (7.9), and ropivacaine (7.10) the ester local anesthetics include cocaine (7.11), procaine (7.12), benzocaine (7.13), and tetracaine (7.14). Since the pharmacodynamic interaction of both amide and ester local anesthetics with the same Na" channel receptor is essentially idenhcal, the amide and ester functional groups are bioisosterically equivalent. However, amide and ester local anesthetics are not equal from a pharmacokinetic perspective. Since ester links are more susceptible to hydrolysis than amide links. [Pg.416]

Deltsidou A (2001). Cocaine abuse in pregnancy. Review of Clinical Pharmacology and Pharmacokinetics International Edition, 15, suppl 225-32... [Pg.154]

Donovan JL, DeVane CL, Malcolm RJ, Mojsiak J, Nora-Chiang C, Elkashef A Taylor RM (2005). Modafinil influences the pharmacokinetics of intravenous cocaine in healthy cocaine-dependent volunteers. Clinical Pharmacokinetics, 44, 753-65... [Pg.154]

Cook, C.E., Pyrolytic characteristics, pharmacokinetics, and bioavailability of smoked heroin, cocaine, phencyclidine and methamphetamine, NIDA Research Monograph 99, 6-23. DHHS Pub. No. 1990. [Pg.31]

Perez-Reyes et al.8 estimated that only 32% of a dose of cocaine base placed in a pipe is actually inhaled by the smoker. Cone9 compared the pharmacokinetics and pharmacodynamics of cocaine by the intravenous, intranasal, and smoked routes of administration in the same subjects. Venous plasma cocaine concentrations peaked within 5 min by the intravenous and smoked routes. Estimated peak cocaine concentrations ranged from 98 to 349 ng/ml and 154 to 345 ng/ml after intravenous administration of 25-mg cocaine hydrochloride and 42-mg cocaine base by the smoked route, respectively. After dosing by the intranasal route (32 mg cocaine hydrochloride) estimated peak plasma cocaine concentrations ranged from 40 to 88 ng/ml after 0.39 to 0.85 h.9 In this study, the average bioavailability of cocaine was 70.1% by the smoked route and 93.7% by the intranasal route. Jenkins et al.10 described the correlation between pharmacological effects and plasma cocaine concentrations in seven volunteers after they had smoked 10 to 40 mg cocaine. The mean plasma... [Pg.39]

A two-compartment open linear model has been described for the pharmacokinetic profile of cocaine after intravenous administration.14 The distribution phase after cocaine administration is rapid and the elimination half-life estimated as 31 to 82 min.14 Cone9 fitted data to a two-compartment model with bolus input and first-order elimination for the intravenous and smoked routes. For the intranasal route, data were fitted to a two-compartment model with first-order absorption and first-order elimination. The average elimination half-life (tx 2 3) was 244 min after intravenous administration, 272 min after smoked administration, and 299 min after intranasal administration. [Pg.40]

Pharmacokinetics Amphetamines are completely absorbed from the gastrointestinal tract, metabolized by the liver, and excreted in the urine. Amphetamine abusers often administer the drugs by intravenous injection and by smoking. The euphoria caused by amphetamine lasts 4 to 6 hours, or 4 to 8 times longer than the effects of cocaine. The amphetamines produce addiction—dependence, tolerance and drug-seeking behavior. [Pg.115]

Volkow ND, Ding U, Fowler JS, Wang GJ, Logan J, Gatley JS, Dewey SL, Ashby C, Lieberman J, Hitzemann R, Wolf AP (1995) Is methylphenidate like cocaine Studies on their pharmacokinetics and distribution in human brain. Arch Gen Psychiatry 52 456 463. [Pg.392]

Cocaine was also the first aminoester local anesthetic, and its adverse effects differ from those of other local anesthetics. Owing to its rapid absorption by mucous membranes, cocaine applied topically can cause systemic toxic effects. There is a wide variation in the rate and amount of cocaine that is systemically absorbed. This variability can be affected by the type and concentration of vasoconstrictor used with cocaine and also accounts for the differences in cocaine pharmacokinetics in cocaine abusers (SEDA-20,128). [Pg.489]

Cone, E. J., Pharmacology and pharmacokinetics of cocaine in hair, presented at the Society of Forensic Toxicology Conference on Drug Testing in Hair, Tampa, FL, Oct. 29-30, 1994. To be published by National Institute on Drug Abuse. [Pg.263]

The inherent difficulties in antagonizing a blocker Hke cocaine have led to the development of a pharmacokinetic approach that aims at acting directly on the drug itself to alter its distribution or accelerate its clearance [7-14]. Pharmacokinetic antagonism of cocaine could be implemented by administration of a molecule, such as an anti-cocaine antibody, that binds tightly to cocaine so as to prevent it from crossing the blood-brain barrier [ 15-20]. [Pg.110]

The blocking action could also be implemented by administration of an enzyme or a catalytic antibody (regarded as an artificial enzyme) that not only binds but also accelerates cocaine metabolism and thereby frees itself for further binding [16-25]. Usually, a pharmacokinetic agent would not be expected to across the blood-brain barrier and thus would itself have no direct pharmacodynamic action, such as abuse liability [5]. [Pg.110]


See other pages where Cocaine pharmacokinetics is mentioned: [Pg.113]    [Pg.113]    [Pg.197]    [Pg.82]    [Pg.96]    [Pg.25]    [Pg.35]    [Pg.478]    [Pg.954]    [Pg.449]    [Pg.611]    [Pg.103]    [Pg.218]    [Pg.21]    [Pg.128]    [Pg.40]    [Pg.42]    [Pg.42]    [Pg.150]    [Pg.374]    [Pg.135]    [Pg.229]    [Pg.59]    [Pg.526]    [Pg.358]    [Pg.358]    [Pg.359]    [Pg.110]    [Pg.111]   
See also in sourсe #XX -- [ Pg.38 , Pg.41 ]




SEARCH



With cocaine pharmacokinetics

© 2024 chempedia.info