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Morphine excretion

Urinary excretion during the first 6 hr. accounted for 29-74 % of the injected morphine, and for 56-91 % at 24 hr. (see Table 5). Three of the 5 subjects excreted 5-7 % during the 2nd day and all excreted small amounts the 3rd day. The addict excreted morphine at the most rapid rate and had the greatest urine output. Nontolerant subjects excreted 7-10% of the dose in the feces in 3-4 days. In contrast, the feces of the addict contained only a negligible amount of radioactivity. [Pg.65]

Thus the addict is excreting morphine more rapidly in the urine and is converting morphine more rapidly to carbon dioxide than does a normal subject. About 1/17 of the injected morphine is accounted for in the expired air of the addict in 24 hr. and only 1 /30 in the expired air of the normal subject. There has been a 50% increase in the ability of the addict to convert the methyl group of morphine to carbon dioxide as compared with a normal subject. The ability to excrete morphine residues has been increased about 20 %. However, the increase in the ability to excrete morphine residues in the urine accounts for 8 times as much of the increased ability of the addict to handle morphine, as does the increased ability to oxidize the methyl group of morphine. (Little can be said at present of the fate of the normorphine residue on loss of the methyl group. There also faintly remains the possibility that transmethylation between the N-methyl of morphine and some methyl donor such as choline may be involved, and that a conversion of morphine to normorphine or other nor-residue may not occur.)... [Pg.72]

Opioids are easily absorbed subcutaneously and intramuscularly, as well as from the gastrointestinal tract, nasal mucosa (e.g., when heroin is used as snuff), and lung (e.g., when opium is smoked). About 90% of the excretion of morphine occurs during the first 24 hours, but traces are detectable in urine for more than 48 hours. Heroin (diacetyhnorphine) is hydrolyzed to monoacetylmorphine, which is then hydrolyzed to morphine. Morphine and monoacetylmorphine are responsible for the pharmacologic effects of heroin. Heroin produces effects more rapidly than morphine because it is more lipid soluble and therefore crosses the blood-brain barrier faster. In the urine, heroin is detected as free morphine and morphine glucuronide (Gutstein and Akil 2001 Jaffe et al. 2004). [Pg.63]

Morphine and its derivatives continue to be considered the gold standard for alleviating pain. Morphine is metabolized in the liver via N-dealkylation and glu-coronidation at the third (M3G) or sixth position (M6G). Although M3G are the most common metabolites (accounts for 50% of the metabolites produced), they elicit no biological activity when bound to MOR. It is the M6G metabolite (accounts for 10% of the metabohtes produced) that elicits the nociceptive/analgesic effect upon binding to the p opioid receptor (Dahan et al. 2008). M6G is predominately eliminated via renal excretion. [Pg.341]

The answer is a. (Hardman, pp 16-20.) Sodium bicarbonate is excreted principally in the urine and alkalinizes it. Increasing urinary pH interferes with the passive renal tubular reabsorption of organic acids (such as aspirin and phenobarbital) by increasing the ionic form of the drug in the tubular filtrate. This would increase their excretion. Excretion of organic bases (such as amphetamine, cocaine, phencyclidine, and morphine) would be enhanced by acidifying the urine. [Pg.275]

In the case of heroin, the indicator used is nonexclusive of heroin consumption, as it is also excreted to a high extent after administration of therapeutic morphine and in minor proportions after use of other opioids, such as codeine, pholcodine, and ethylmorphine. In order to obtain comparable results to previous studies [25, 31], an average medical administration of morphine of 10 mg/capita/year [45] and an excretion rate of 85% of morphine after therapeutic use [25, 31] were considered in the calculations. [Pg.201]

In mammals, phenobarbital and phenytoin increase serum ceruloplasmin concentrations (Aaseth and Norseth 1986). Chronic copper poisoning in sheep is exacerbated when diets contain heliotrope plants (Heliotropium sp., Echium spp., Senecio sp.). Aggravated effects of the heliotrope plants include reduced survival and a twofold to threefold increase in liver and kidney copper concentrations when compared to control animals fed copper without heliotropes (Howell et al. 1991). Rats given acutely toxic doses of 2,3,7,8-tetrachlorodibenzo-para-dioxin had elevated concentrations of copper in liver and kidney because of impaired biliary excretion of copper (Elsenhans et al. 1991). Morphine increases copper concentrations in the central nervous system of rats, and dithiocarbam-ates inhibit biliary excretion (Aaseth and Norseth 1986). In human patients, urinary excretion of copper is increased after treatment with D-penicillamine, calcium disodium EDTA, or calcium trisodium diethylenetriamine penta acetic acid (Flora 1991). [Pg.139]

Pentazocine has been successfully used to relieve labour pain [201] and its obstetric use in place of pethidine is favoured by,its apparent inferior ability to pass the placental barrier [206]. A clinical trial of (+)- and (-)-pentazocine adds to the rare number of examples in which optical enantiomorphs have been evaluated [207]. In post-operative patients, response to 60 mg of the dextro isomer was less than that to 5 mg of morphine, while 25—29 mg of (-)-pentazocine was as effective as 10 mg of morphine. Hence most of the activity of the race-mate resides in the laevo isomer, as anticipated from results in animals [208]. Several studies of the distribution, excretion and metabolism of pentazocine have been made. Peak levels of the tritium-labelled drug (and its c/s-3-chloroallyl analogue) were present in the C.N.S. of a cat within 40 minutes of intramuscular administration [209], the comparable figure for morphine being 2 hours [210]. [Pg.257]

Drugs must also be considered as foreign compounds, and an essential part of drug treatment is to understand how they are removed from the body after their work is completed. Glucuronide formation is the most important of so-called phase II metabolism reactions. Aspirin, paracetamol, morphine, and chloramphenicol are examples of drugs excreted as glucuronides. [Pg.489]

The majority of their metabolites are inactive with a few notable exceptions, such as morphine-6-glucuronide, which produces an analgesic effect normeperidine and norpropoxyphene, which produce excitatory but not analgesic effects and 6-(3-naltexol, which is less active than naltrexone as an antagonist but prolongs the action of naltrexone. Excretion of the metabolites requires adequate renal function, since excretion by routes other than the urine are of minor importance. [Pg.319]

Pharmacokinetics Variably absorbed from the GI tract. Protein binding low. Metabolized in liver. Primarily excreted in urine as morphineglucuronide con j ugates and unchanged drug—morphine, codeine, papaverine, etc. Unknown if removed by hemodialysis. Half-life 2-3 hr. [Pg.937]

Tubular secretion The active secretory systems can rapidly remove the protein-bound drugs from the blood and transport them into tubular fluid as the drugs that are bound to proteins are not readily available for excretion by filtration. The drugs known to be secreted by organic anion secretory system (i.e. strong acids) are salicylates, chlorothiazide, probenecid, penicillin etc. and cation (i.e. bases) includes catecholamines, choline, histamine, hexamethonium, morphine etc. [Pg.35]

Morphine orally is less effective and absorption is very slow. It has variable and high first pass metabolism when given by subcutaneous route, its analgesic effect starts within 10 minutes which persists for 4 to 5 hours and by IV route, it produces immediate action. In plasma, it binds to plasma proteins (approx. 30%). In liver it is metabolized by conjugation to glucuronic acid to form active and inactive products, which are excreted in urine. It is also excreted though bile and in the faeces. [Pg.77]

Enhancing excretion of unabsorbed morphine from the intestine. [Pg.78]

Acidify the urine to enhance the renal excretion of morphine. [Pg.78]

Once absorbed, foreign compounds may react with plasma proteins and distribute into various body compartments. In both neonates and elderly human subjects, both total plasma-protein and plasma-albumin levels are decreased. In the neonate, the plasma proteins may also show certain differences, which decrease the binding of foreign compounds, as will the reduced level of protein. For example, the drug lidocaine is only 20% bound to plasma proteins in the newborn compared with 70% in adult humans. The reduced plasma pH seen in neonates will also affect protein binding of some compounds as well as the distribution and excretion. Distribution of compounds into particular compartments may vary with age, resulting in differences in toxicity. For example, morphine is between 3 and 10 times more toxic to newborn rats than adults because of increased permeability of the brain in the newborn. Similarly, this difference in the blood-brain barrier underlies the increased neurotoxicity of lead in newborn rats. [Pg.162]

The mechanisms underlying (he development of tolerance are not fully understood. Biochemically, it may he attractive to explain tolerance by decreased absorption, altered distribution, increased biotransfomiatiun, and/or increased excretion of the drug However, these processes have been shown to he unrelated to (he development of tolerance. Thus, cellular adaptation offers the greatest likelihood for clarifying the phenomenon. Evidence for cellular adaptation is the finding that (he respiration of chemically stimulated cortical slices of brain front normal rats is markedly deptessed by morphine, whereas the respiration of those from rats chronically dosed with morphine is unaffected... [Pg.1042]


See other pages where Morphine excretion is mentioned: [Pg.291]    [Pg.291]    [Pg.101]    [Pg.262]    [Pg.212]    [Pg.89]    [Pg.22]    [Pg.524]    [Pg.269]    [Pg.83]    [Pg.406]    [Pg.74]    [Pg.90]    [Pg.489]    [Pg.156]    [Pg.41]    [Pg.56]    [Pg.6]    [Pg.90]    [Pg.36]    [Pg.79]    [Pg.80]    [Pg.36]    [Pg.284]    [Pg.284]    [Pg.683]    [Pg.683]    [Pg.427]    [Pg.52]    [Pg.55]   
See also in sourсe #XX -- [ Pg.52 ]




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Excretion of Free Morphine in Urine

Morphine biliary excretion

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