Big Chemical Encyclopedia

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

Articles Figures Tables About

Atropine pharmacokinetics

Aaltonen L, Kanto J, Iisalo E, Pihlajamaki K (1984) Comparison of radioreceptor assay and radioimmunoassay for atropine pharmacokinetic application. Eur J Clin Pharmacol 26 613-617... [Pg.343]

L. Aaltonen, J, Kanto, E. lisalo, and K. Pihlajamaki, Comparison of radioreceptor assays and radioimmunoassay for atropine Pharmacokinetic application, Eur.. Clin. Pharmacol, 26 613-617 (1984). [Pg.64]

Mechanism of Action Competitive inhibitors of the muscarinic actions of acetylcholine, acting at receptors located in exocrine glands, smooth and cardiac muscle, and intramural neurons. Composed of 3 main constituents atropine, scopolamine, and hyoscyamine. Scopolamine exerts greater effects on the CNS, eye, and secretory glands than the constituents atropine and hyoscyamine. Atropine exerts more activity on the heart, intestine, and bronchial muscle and exhibits a more prolonged duration of action compared to scopolamine. Hyoscyamine exerts similar actions to atropine but has more potent central and peripheral nervous system effects. TherapeuticEffect Peripheral anticholinergic and antispasmodic action, mild sedation. Pharmacokinetics None known... [Pg.121]

Mechanism of Action Ananticholinergicthat exerts antispasmodic (papaverine-like) and antimuscarinic (atropine-like) action on the detrusor smooth muscle of the bladder. Therapeutic Effect Increases bladder capacity and delays desire to void. Pharmacokinetics ... [Pg.922]

Atropine is the racemic mixture of R- and S-hyoscyamine produced during the pharmaceutical plant extraction process. R-hyoscyamine is nearly inactive on MR (distomer) whereas S-hyoscyamine exhibits high affinity (eutomer). Nevertheless, due to economic reasons atropine is typically administered even though only half of the applied dose (S-hyoscyamine) is pharmacologically active on MR. Surprisingly, there is still little information about different pharmacokinetic behaviour of both enantiomers anyhow [46,47],... [Pg.297]

Kentala E, Kaila T, Iisalo E, Kanto J (1990) Intramuscular atropine in healthy volunteers a pharmacokinetic and pharmacodynamic study. Int J Clin Pharmacol Ther Toxicol... [Pg.343]

Pharmacokinetics Atropine is readily absorbed, partially metabolized by the liver, and is eliminated primarily in the urine. It has a half-life of about 4 hours... [Pg.58]

Pharmacokinetics and adverse effects These aspects are similar to those of atropine. [Pg.59]

The only compound in this group whose fate In the body has been studied to a moderately satisfactory extent Is atropine. Some Information on the metabolic fates of B- ulnuclldinyl benzllate and of dlethylamlnoethyl benzllate Is available (193, 219), but It does not account completely for all parts of the molecules. The binding of 3-qulnuclldlnyl benzllate to nerve cells (193,194) and to organelles from such cells (195) has been studied, but no detailed studies, of Its detoxification, pharmacokinetics, and molecular pharmacology have been found for use In this review. Little or no Information on the biochemical aspects of the activities of the anticholinergic compounds surveyed here has been found. Whether such Information exists In literature that has been withheld from consideration for this survey Is unknown. [Pg.239]

Pharmacokinetics. Atropine is readily absorbed from the gastrointestinal tract and may also be injected by the usual routes. The occasional cases of atropine poisoning following use of eye drops are due to the solution rurming down the lacrimal ducts into the nose and being swallowed. Atropine is in part destroyed in the liver and in part excreted unchanged by the kidney (t 2 h). [Pg.443]

Example Diphenoxylate with atropine Route Pregnancy Pharmacokinetic (Lomotil) Schedule V PO category C Well absorbed from GI tract metabolized in liver eliminated in feces... [Pg.275]

Clement JG, Bailey DG, Madill HD et al. (1995). The acetylcholinesterase oxime reactivator HI-6 in man pharmacokinetics and tolerability in combination with atropine. Biopharm Drug Disposit, 16, 415 125. [Pg.323]

Thiermann H, Spohrer U, Klimmek R et al. (1995b). Pharmacokinetics of atropine and its combination with HI 6 or HLo 7 in dogs after i.m. injection with newly developed dry/wet autoinjectors. Przeg Lek, 52, 208. [Pg.328]

Pharmacokinetics of atropine Atropine is the prototypical nonselective muscarinic blocker. This alkaloid is found in Atropa belladonna and many other plants. Because it is a tertiary amine, atropine is relatively lipid-soluble and readily crosses membrane barriers. The drug is well distributed into the CNS and other organs and is eliminated partially by metabolism in the liver and partially by renal excretion. The elimination half-life is approximately 2 hours, and the duration of action of normal doses is 4-8 hours except in the eye, where effects last for 72 hours or longer. [Pg.69]

A. Prototypes and Pharmacokinetics Atropine and other naturally occurring belladonna alkaloids were used for many years in the treatment of asthma with only modest benefits. A quaternary antimuscarinic agent designed for aerosol use, ipratropium, has achieved much greater success. This drug is dehvered to the airways by pressurized tierosol. When absorbed, ipratropium is rapidly metabolized and has little systemic action. [Pg.187]

Hindcrling, P. H., Gundert-Remy, U., and Schmidlin, O. (1985). Imegraied pharmacokinetics and pharmacodynamic.s of atropine in healthy humans. I Pharmacokinetics. J. Pharm. Set. 74, 703-710. [Pg.729]

Kamo. J., Vinanen, R., Ii.sulo, E., Maenpaa, K., and Liukko, P, (1981). Placental iran.sfer and pharmacokinetics of atropine after a single maternal intravenous and intramuscular administration, Acta Aiiaesthe.slol. Scand. 25, 85-88. [Pg.730]

As stated, a number of PBPK/PD models have been developed for individual nerve agents (sarin, VX, soman, and cyclosarin) in multiple species. Chapter 58 in the current volume discusses tiie development of such models. Standalone PBPK or compartmental models have also been developed that describe the pharmacokinetics of certain countermeasures, such as diazepam (Igari et al., 1983 Gueorguieva et al., 2004) and oximes (Stemler et al., 1990 Sterner et al., 2013). However, to date, few models for specific countermeasures have been harmonized and linked to NA PBPK/PD models to be able to quantitatively describe their pharmacokinetic and pharmacodynamic interactions. This is partly due to the fact that most PBPK/ PD models developed for NAs and other OPs focus on the inhibition of ChEs as the critical endpoint. The lack of a mathematical description of the disruption of other complex biochemical pathways presents a problem for linking these NA models to those of many countermeasures. For example, the conventional NA countermeasures, atropine and diazepam, as well as many novel countermeasures, do not directly impact ChE kinetics because they act at sites distinct from the active site of the esterases, such as muscarinic, GABA, or NMDARs (Figure 69.2). [Pg.1041]


See other pages where Atropine pharmacokinetics is mentioned: [Pg.316]    [Pg.317]    [Pg.298]    [Pg.1288]    [Pg.326]    [Pg.275]    [Pg.358]    [Pg.358]    [Pg.359]    [Pg.957]    [Pg.989]    [Pg.1044]    [Pg.73]    [Pg.38]    [Pg.111]    [Pg.159]    [Pg.191]    [Pg.335]    [Pg.202]    [Pg.1119]    [Pg.720]    [Pg.732]    [Pg.38]    [Pg.246]    [Pg.640]    [Pg.156]   
See also in sourсe #XX -- [ Pg.69 ]

See also in sourсe #XX -- [ Pg.718 ]

See also in sourсe #XX -- [ Pg.382 ]




SEARCH



Atropine

Atropinism

© 2024 chempedia.info