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Biomedical subjects

E M Faed

Publications and source records attributed to E M Faed.

11 recordsLinked to original sources
PubMed1984

Glucuronidation and elimination of diflunisal in the isolated perfused rat liver: effect of pretreatment with phenobarbitone, clofibric acid and spironolactone.

The effects of pretreatment of rats with phenobarbitone, clofibric acid and spironolactone on the metabolism and biliary excretion of the salicylate derivative diflunisal have been studied using the isolated perfused liver. The clearance of diflunisal was increased significantly by pretreatment with each of the drugs. Biliary excretion of diflunisal acyl and phenolic glucuronides followed apparent first-order and Michaelis-Menten kinetics, respectively. Pretreatment with clofibric acid or spironolactone resulted in a significant increase in the biliary excretion of the phenolic glucuronide. Pretreatment with phenobarbitone or spironolactone enhanced biliary excretion of the acyl glucuronide, particularly during the first 2 hr. The concentration of the phenolic glucuronide in the perfusate increased steadily during the 6 hr perfusions, whereas the acyl glucuronide concentration was relatively stable, reflecting the ease of hydrolysis of acyl glucuronides under physiological conditions.

Animals↗
PubMed1981

Protein binding of drugs in plasma, interstitial fluid and tissues: effect on pharmacokinetics.

Drug binding in the interstitial fluid as well as in the plasma must be taken into account when considering the pharmacokinetics of drugs which are highly bound to plasma proteins and have a relatively small apparent volume of distribution (V). The half-life and apparent volume of distribution of such a drug can be affected significantly by changes in the extent of binding of the drug in both the plasma and the interstitial fluid. An alteration in the fraction of drug in the tissues which is unbound will primarily affect the pharmacokinetics of drugs which have a relatively large apparent volume of distribution. The effect of changes in the plasma free fraction of drug (fP) on tissue binding can be deduced from a plot of fP versus V, but not from a plot of fP versus beta.

Blood Proteins↗
PubMedDate not supplied

Separation of two conjugates of clofibric acid (CPIB) found in the urine of subjects taking clofibrate.

1. Two main conjugates of CPIB (2-[chlorophenoxy]-2-methylpropionic acid) are present in the urine of subjects taking clofibrate. The metabolites can be separated by thin-layer chromatography (TLC). 2. Both conjugates are hydrolysed by dilute alkali, but only one is hydrolysed by the enzyme beta-glucuronidase. In eighty-five urine specimens this conjugate accounted for an average of 54.5% (range 25-70%) of the total CPIB, while 2.6-12.45% (mean 5.1%) was present as free CPIB.

Chromatography, Gas↗
PubMedDate not supplied

Measurement of clofibric acid (CPIB) metabolites in plasma of patients on clofibrate therapy.

1. The metabolites of clofibric acid [CPIB;2-(chlorophenoxy)-2-methylpropionic acid] are present in the plasma of patients on clofibrate therapy. The highest plasma concentrations of CPIB in metabolite form (up to 51 micrograms/ml) were generally found in patients with renal disease. Negligible concentrations (less than or equal to 2 micrograms/ml) were found in only seven patients out of thirty-six studied. 2. The two conjugates of CPIB found in urine were present in plasma. 3. When measuring conjugated CPIB in plasma it is essential to take care in the handling and storage of specimens, and to select an assay method known to be specific for unmetabolized CPIB.

Clofibrate↗