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  • 1
    ISSN: 1573-739X
    Keywords: Chromatography, high pressure liquid ; Clearance ; Metabolism ; Nalidixic acid ; Pharmacokinetics ; Protein binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Nalidixic acid is metabolized by hydroxylation to 7-hydroxymethylnalidixic acid∥ and then by oxidation to 7-carboxynalidixic acid.∥ The half-lives of the two elimination phases of nalidixic acid are 0.75 and 2.5 h. The apparent half-lives of the metabolite 7-hydroxymethylnalidixic acid are 2.5 and 5.5 h. Plasma protein binding of nalidixic acid is 95% and that of 7-hydroxymethylnalidixic acid 65%. The renal clearance of nalidixic acid varies between 2 and 25 ml/min and that of 7-hydroxymethylnalidixic acid between 37 and 162 ml/min. Of nalidixic acid 42% is glucuronidated and 40% hydroxylated. Of the hydroxy metabolite 57% is glucuronidated and 32% excreted unchanged. 7-Carboxynalidixic acid is excreted in the urine and is not glucuronidated. The variations in the glucuronidation/ hydroxylation ratio of nalidixic acid and the glucuronidation/renal excretion ratio of the 7-hydroxymethyl metabolite belong to a normal distribution.
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  • 2
    ISSN: 1573-739X
    Keywords: Drug interactions ; Enoxacin ; Metabolism ; Ofloxacin ; Pharmacokinetics ; Theophylline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract The pharmacokinetic parameters of theophylline and its major metabolites were measured in two healthy volunteers, after the administration of theophylline alone and during co-medication with ofloxacin, 200 mg twice daily, or enoxacin, 200 mg twice daily. During enoxacin co-medication, elimination half-lives of theophylline increased from 8.7 h to 17.4 h and from 6.1 h to 12.3 h, respectively. As the renal clearance of theophylline did not change, the decreased elimination of theophylline during enoxacin co-medication must result from a reduced metabolic clearance. Enoxacin co-medication caused a clearly decreased formation of the metabolitesI-methyluric acid and 3-methylxanthine, formed by N-demethylation, whereas the C-8 oxidation of theophylline was less influenced compared to the blank. Enoxacin's interference with the theophylline disposition is predominantly based on the inhibition of the microsomal N-demethylation. Ofloxacin co-medication did not induce a change in the plasma parameters or renal excretion of theophylline and its metabolites.
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  • 3
    ISSN: 1573-739X
    Keywords: Chromatography, high pressure liquid ; Clearance ; Metabolism ; Pharmacokinetics ; Sulfaphenazole
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract A direct high pressure liquid chromatographic analysis of sulfaphenazole-N2-glucuronide in urine is described. After an oral dose of 439 mg of sulfaphenazole, 0% is excreted unchanged in the urine, 〈 1% is excreted as N4-acetylsulfaphenazole. As N2-glucuronide 49.4% is excreted in one slow acetylator and 84.8% in one fast acetylator.
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  • 4
    ISSN: 1573-739X
    Keywords: Analgesics ; Injections, intrathecal ; Metabolism ; Narcotics ; Nicomorphine ; Pharmacokinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract In ten patients who received an epidural injection of 15 mg of nicomorphine, the compound was relatively slowly released from the epidural space and was found in plasma for approximately 1.5 h. Nicomorphine is relatively slowly metabolized into 6-nicotinoylmorphine and morphine. The rate of release is patient-dependent. The relative AUC values are 15.3% for nicomorphine, 23.9% for 6-nicotinoylmorphine and 60.8% for morphine. The mean clinical effect lasts for 18.2±10.1 h.
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  • 5
    ISSN: 1573-739X
    Keywords: Chromatography, high pressure liquid ; Clearance ; Metabolism ; Pharmacokinetics ; Protein binding ; Sulfadimethoxine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Sulfadimethoxine is metabolized byO-dealkylation, N4-acetylation and N1-glucuronidation. In man, only N1-glucuronidation and N4-acetylation takes place, leading to the final double conjugate N4-acetylsulfadimethoxine-N1-glucuronide. The N1-glucuronides are directly measured by high pressure liquid chromatography. When N4-acetylsulfadimethoxine is administered as parent drug, 30% of the dose is N1-glucuronidated and excreted. Fast acetylators show a shorter half-life for sulfadimethoxine than slow acetylators (27.8±4.2 h versus 36.3±5.4 h; P=0.013), similarly the half-life of the N4-acetyl conjugate is also shorter in fast acetylators (41.3±5.2 h versus 53.5±8.5 h, P=0.036). No measurable plasma concentrations of the N1-glucuronides from sulfadimethoxine are found in plasma. N1-glucuronidation results in a 75% decrease in protein binding of sulfadimethoxine. N4-acetylsulfadimethoxine and its N1-glucuronide showed the same high protein binding of 99%. Approximately 50–60% of the oral dose of sulfadimethoxine is excreted in the urine, leaving 40–50% for excretion into bile and faeces.
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  • 6
    ISSN: 1573-739X
    Keywords: Ascorbic acid ; Cimetidine ; Cytochrome P-450 ; Hydrocortisone ; Metabolism ; Steroid hydroxylases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract A blind, parallel, prospective, clinical study was conducted to investigate the effect of ascorbic acid on human serum hydrocortisone concentrations which were decreased by the administration of cimetidine. The study population included 16 male adults scheduled for major abdominal vascular surgery. The study was conducted in surgical patients under anaesthesia, in which steroidogenesis was inhibited by cimetidine. The results showed a reduction in serum hydrocortisone concentrations in patients receiving a placebo. In patients receiving ascorbic acid, there was a significant increase in serum hydrocortisone concentration. This reflects the normal serum hydrocortisone profile for this operation and anaesthetic technique. Cimetidine can bind to cytochrome P-450 covering the active haem group, the cytochrome proves to be of vital importance for hydroxylation reactions, involved in human steroidogenesis. Serum hydrocortisone concentrations will decrease when cytochrome P-450 becomes blocked. Intravenous administration of ascorbic acid was supposed to cause relief for this decrease. The reasons are undetermined yet. This investigation proved that ascorbic acid can prevent cimetidine-induced decrease of human serum hydrocortisone concentrations.
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  • 7
    ISSN: 1573-739X
    Keywords: Chemistry, analytical ; Chromatography, high pressure liquid ; Drug stability ; Pharmacokinetics ; Vinblastine ; Vincristine ; Vindesine ; Vinzolidine ; Adjuvants, immunologie ; Anti-inflammatory agents ; Azadirachta indica A. Juss ; Chemistry, analytical ; Pharmacognosy ; Anaesthesia, epidural ; Anaesthesia, intrathecal ; Bupivacaine ; Hemostasis ; Antioxidants ; Butylated hydroxyanisole ; Butylated hydroxytoluene ; Food additives ; Metabolism ; Neoplasms ; Toxicology ; Bronchodilator agents ; Isozymes ; Milrinone ; Phosphodiesterase ; Sulmazole
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1573-739X
    Keywords: Clearance, renal ; Glucuronates ; Metabolism ; Pharmacokinetics ; Probenecid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Probenecid shows dose-dependent pharmacokinetics. When in one volunteer the dose is increased from 250 to 1,500 mg orally, thet 1/2 increased from 3 to 6 h. TheC max was 14μg/ml with a dosage of 250 mg, 31μg/ml with 500 mg, 70μg/ml with 1,000 mg and 120μg/ml with 1,500 mg. Thet max remained 1 h for all four dosages. The AUC/dose ratio increased with the dose, indicating nonlinear elimination. The total body clearance declined from 64.5 ml/min for 250 mg to 26.0 ml/min for 1,500 mg. The renal clearance of probenecid remained constant, 0.6–0.8 ml/min. Protein binding of probenecid is high (91%) and independent of the dose. The phase I metabolites show lower protein binding values (34–59%). The protein binding of probenecid glucuronidein vitro (spiked plasma) is 75%. Probenecid is metabolized by cytochrome P-450 to three phase I metabolites. Each of the metabolites accounts for less than 10% of the dose administered; the percentage recovered in the urine is independent of the dose. The main metabolite probenecid glucuronide is only present in urine and not in plasma. The renal excretion rate-time profile of probenecid glucuronide shows a plateau value of approximately 700μg/min (46 mg/h) with acidic urine pH. The duration of this plateau value depends on the dose: 2 h at 500 mg, 10 h at 1,000 mg and 20 h at 1,500 mg. It is demonstrated that probenecid glucuronide must be formed in the kidney during its passage of the tubule. The plateau value in the renal excretion rate of probenecid value reflects itsV max of formation.
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Pharmacy world & science 16 (1994), S. 69-76 
    ISSN: 1573-739X
    Keywords: Adenosine ; Biological transport ; Heart ; Ischemia ; Metabolism ; Myocardial reperfusion injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Adenosine has recently received much attention for the protection it provides against the deleterious effects of ischaemia reperfusion. Whenever the demand for oxygen exceeds its supply, adenosine triphosphate in myocytes is rapidly dephosphorylated to adenosine. Adenosine may then protect the myocardium against ischaemia-reperfusion damage. However, the accumulation of adenosine is limited by its rapid uptake and catabolism in the endothelium and in red blood cells. The strict compartmentalization of the enzyme pathways involved in the metabolism ofadenosine, e.g. adenosine production by myocytes, its pharmacological action in the interstitium, its catabolism in the endothelium and in red blood cells, and its carrier-mediated transport across membranes, provides a unique target for pharmacological interventions. Blockade of adenosine uptake may indeed result in prolonged adenosine accumulation specifically in those regions of the heart where it is produced. In recentyears considerable evidence has been gathered on the adenosine-mediated cardioprotective actions of nucleoside transport inhibitors.
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Pharmacy world & science 9 (1987), S. 50-55 
    ISSN: 1573-739X
    Keywords: Absorption ; Adult ; Aged ; Child ; Clearance ; Metabolism ; Pharmacokinetics ; Protein binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Age significantly affects therapeutics in both general and specific ways. In newborns and in infants various physiological processes are still developing, whereas in elderly there may be decreased efficiency or capacity of physiological processes. Unexpected or ‘idiosyncratic’ responses to drugs in the very old or in the very young often can be explained by age-related changes in absorption, distribution, metabolism, end-organ responsiveness and excretion. Adolescence is often associated with rapid growth and changing body composition. Special problems with adolescents are poor compliance and drug abuse. Adults show a rather stable pharmacokinetic profile, although the cardiac output diminishes and the peripheral resistance increases about 1% annually. Exposure to enzyme-inducing agents (nicotine, cimetidine) influences the pharmacokinetic parameters of both adolescents and adults.
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