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Biomedical subjects

J Edelson

Publications and source records attributed to J Edelson.

At least 37 records · Page 2Linked to original sources
PubMed1983

Determination of azarole plus its reduction product by HPLC.

An analytical methodology for the assay of azarole plus its reduced product in plasma was developed. The method consists of oxidation of the sample with potassium ferrocyanide, extraction, and subsequent analysis by high performance liquid chromatography. Assays of prepared plasma samples demonstrated an overall precision of +/- 6.2%; accuracy ranged from -9.1% low to 5.1% high, based on mean values at several concentrations. Analysis of variance for the effects of concentration, time, and the interactive term concentration X time were all insignificant.

Chromatography, High Pressure Liquid↗
PubMed1982

Pharmacokinetics of rosoxacin in human volunteers.

Reversed-phase liquid chromatography was used to determine plasma rosoxacin concentrations in normal, healthy males, each of whom received one 300 mg capsule of rosoxacin. The plasma data for each subject were described by an open one-compartment body model with first-order absorption, and the pharmacokinetic parameters were determined. The mean (+/- SE) apparent first-order terminal elimination rate constant was 0.203 +/- 0.015 hr-1 (N = 16), the mean apparent volume of distribution was 0.644 +/- 0.050 liters/kg, and the mean apparent plasma clearance was 2.08 +/- 0.15 ml/min/kg.

4-Quinolones↗
PubMed1982

Determination of isoetharine in plasma by reversed-phase chromatography with amperometric detection.

A reversed-phase liquid chromatographic method for the determination of isoetharine in blood plasma, utilizing amperometric detection, is described. Plasma samples were extracted utilizing an ion-pair reagent, di-(2-ethylhexyl)phosphoric acid, to concentrate the catecholamine. Only minor differences were observed in the relative bioavailability of isoetharine hydrochloride and isoetharine mesylate after oral administration to rats. Observed plasma levels, at 1 hr after oral medication, were highly variable in dose-ranging studies at doses of 800-2500 mg/kg/day for 2 weeks.

Administration, Oral↗
PubMed1982

Disposition of arildone, an antiviral agent, after various routes of administration.

[14C]arildone was administered both topically and intravaginally to mice 5 times a day for 7 days to simulate conditions of clinical usage. Urinary and fecal excretion of radioactivity indicated that arildone was extensively absorbed by both routes of administration. The levels of radioactivity in the vagina and skin declined from about 12 micrograms equivalents per g to 3 micrograms equivalents per g between 1 and 2 days after the last application. Only small amounts of unchanged arildone were found in urine from the vaginally treated animals; the major urinary metabolites were chloromethoxyphenol, its sulfate ester, and chlorohydroquinone sulfate. After about 1 month of daily oral administration of arildone to rats and monkeys or vaginal administration three times a day for 20 days to dogs, only low levels of intact drug were found in the systemic circulation. The disposition or beta-phase half-life of arildone in monkeys after intravenous administration was about 0.5 h. The disposition of [14C]arildone in mice, rats, dogs, and monkeys after various routes of administration was also investigated.

Administration, Oral↗
PubMed1982

The pharmacokinetics and pharmacodynamics of sulfinalol hydrochloride in dogs after intravenous administration.

The pharmacokinetic behavior of sulfinalol hydrochloride, an antihypertensive agent with vasodilator and beta-adrenergic blocking activity, was determined in dogs after intravenous administration. The plasma concentrations of sulfinalol HCl were fit to an open two-compartment body model. The mean values for the alpha- and beta-phase constants were 33.3 hr-1 and 0.52 hr-1, respectively. The mean plasma clearance was 2.30 L/kg X hr. The steady-state volume of distribution was approximately four times the body weight of the animals. The urine data gave renal clearance rates approximately equal to the normal glomerular filtration rate in the dog. About 7.5% of the administered dose was excreted in the urine as free sulfinalol hydrochloride. The time course of the hypotensive effect of sulfinalol appears to be better correlated with calculated tissue levels of drug than with observed plasma levels.

Adrenergic beta-Antagonists↗
PubMed1982

The disposition of quinfamide in the rat.

The disposition of quinfamide 1-(dichloroacetyl)-6-(2-furoyloxy)-1, 2, 3, 4-tetrahydroquinoline, an enteric anti-amoebic agent, was studied in the rat. A peak blood level equivalent to 2.3 micrograms/ml of quinfamide was observed at 7 hr following a 20 mg/kg oral dose. Urinary recovery of radioactivity was much higher (84%) following intravenous than oral (48%) administration. Drug levels, in all of the tissues examined. were low. The major pathways of quinfamide metabolism in the rat involve hydrolysis of one or both ester groups, acetylation of the de-acylated product to 1-acetyl-1, 2, 3, 4-tetrahydro-6-quinolinol, oxidation of this to the 1-glycolyl metabolite, and aromatization to 6-hydroxyquinoline.

Animals↗
PubMed1981

The analysis of arildone in plasma, urine and feces by gas--liquid chromatography with electron-capture detection.

The analysis of arildone in plasma, urine and feces by gas--liquid chromatography with electron-capture detection is described. O-(2,3,4,5,6-Pentafluorobenzyl)hydroxylamine is the derivatizing agent for the plasma and urine analysis; 3-nitrophenylhydrazine is utilized for fecal analysis. The mean (+/- S.E.) minimum quantifiable level of arildone was 1.4 (+/- .02) ng/ml in urine, 6.4 (+/- 0.1) ng/ml in plasma, and 12.6 (+/- 1.0) ng/g in feces. The chromatographic response was linear in the range of 0 and 10--120 ng/ml for plasma, 0 and 2.5--20 ng/ml for urine and 0 and 25-250 ng/g for feces. The estimated overall precision of the assay was 5.5%, 64% and 8.9% in urine, plasma and feces, respectively.

Antiviral Agents↗
PubMed1981

Concentration of perfluorohexyl bromide in dog plasma and selected tissues.

Beagle dogs received single perfluorohexyl bromide doses, either 30.2 g/kg po or 3.8 g/kg intratracheally. The apparent first-order plasma half-life during the terminal elimination phase was approximately 8 hr after oral treatment and greater than 8 hr after intratracheal administration. Tissue analysis showed the highest mean concentration of the compound in abdominal fat 1 week after intratracheal administration. One dog had detectable levels in abdominal fat 4 weeks after treatment by either administration route.

Administration, Oral↗
PubMed1981

Relationship between amrinone plasma concentration and cardiac index.

Amrinone was given to 14 patients with congestive heart failure as an intravenous bolus (1 mg/sec) at doses ranging from 0.5 to 3.5 mg/kg. Simultaneous determinations of cardiac index were made by thermodilution and of amrinone plasma concentration by high-performance liquid chromatography. A relationship between improvement in cardiac index and increasing plasma concentrations of amrinone was demonstrated for 13 of the 14 patients. The percentage increase in cardiac index correlated with amrinone plasma concentration (r = 0.81; p less than 0.001). Amrinone was given to four patients as an intravenous bolus dose of 1.5 mg/kg followed by a constant infusion of 10 micrograms/kg/min for 10 hr; simultaneous determinations of cardiac index and circulating levels of amrinone indicated that both declined after the initial rise. The plasma concentration of amrinone remained relatively constant during the infusion at about 1.7 micrograms/ml. In all cases, despite the relatively constant plasma levels there was a decline in cardiac index after about 4 to 5 hr of infusion, although the cardiac index remained above the baseline; during the constant infusion the cardiac index rose again and was maintained at a reasonably constant level for the last 3 hr. Seven patients received oral doses of amrinone of about 3 mg/kg, and simultaneous determinations of cardiac index and plasma concentration showed a relationship between amrinone level and rise in cardiac index (p less than 0.05). In 16 patients after amrinone orally sufficient blood samples were taken to estimate the apparent first-order terminal elimination t 1/2. The t 1/2 as estimated by log-linear regression ranged from about 3 to 15 hr; mean +/- SEM value was 8.3 (+/- 1.1) hr.

Aminopyridines↗
PubMed1981

Amrinone metabolism.

High-performance liquid chromatographic methods for the analysis of amrinone in plasma and for both amrinone and its N-acetyl metabolite in urine were developed and applied to measure specimens obtained from a number of healthy men who had received intravenous or oral amrinone. The intravenous doses ranged from 0.8 to 2.2 mg/kg. Terminal elimination of amrinone from the bloodstream followed apparent first-order kinetics. Half-life, after the drug had distributed to the tissues, was estimated by a log-linear least-squares regression; mean half-life was 2.6 +/- 1.4 hr. During the first 24 hr after medication, unchanged amrinone excreted in the urine of these subjects represented 10% to 40% of the dose. N-Acetyl metabolite in the urine represented less than 2% of the dose. In the oral study, doses ranged from 25 to 250 mg (0.31 to 3.5 mg/kg) and the maximum plasma concentration attained was proportional to the dose. The first order terminal elimination half-life was possibly dose-related. In only one subject were there unequivocal amounts of the N-acetyl metabolite in the plasma.

Aminopyridines↗
PubMed1980

Analysis of mepivacaine, bupivacaine, etidocaine, lidocaine, and tetracaine.

A GLC method, employing a nitrogen-phosphorus-sensitive detector, is described for the analysis of mepivacaine, bupivacaine, etidocaine, lidocaine, and tetracaine in biological fluids. The method is simple, reliable, and sensitive, with a practical limit of sensitivity of approximately 2.5 ng/ml, well below therapeutic plasma levels. Extensive start-up procedures and sample preparation are not required.

Acetanilides↗
PubMed1980

Disposition of a series of tetrahydrocarbazoles.

Cyclindole was extensively metabolized and eliminated primarily via the kidneys from most laboratory animals and man. Only in the dog was cyclindole a major urinary component. Cyclindole was metabolized by N-demethylation and/or hydroxylation. In studies utilizing radiolabeled drug, the primary urinary component was polar material which probably resulted from conjugation of the hydroxylated products. When desmethylcyclindole was administered to rats and dogs, large amounts of unchanged drug were administered to rats and dogs, large amounts of unchanged drug were recovered in the urine; there was no 3-aminotetrahydrocarbazole present. Significant amounts of urinary radioactivity were thought to represent hydroxylated and/or conjugated products. When 7-hydroxycyclindole was administered to dogs, only free parent drug was recovered from the urine; there was no evidence for N-demethylation. Flucindole, the 6,8-difluoro analog of cyclindole was metabolized by dog and man via N-demethylation with the formyl derivative being a probable intermediate in this reaction; both products were found in the urine. No didesmethyl metabolite was detected. In contrast to cyclindole, the N-oxide of flucindole was found in urine from both species. The route of elimination of oxarbazole and its metabolites was species specific: urinary excretion was 96.5, 38.7, 24.5, and 2.0% for the guinea pig, monkey, rat, and dog, respectively. The major urinary metabolite was O-demethyl oxarbazole; this metabolite was conjugated in all species except the guinea pig. The dog and monkey excreted small quantities of conjugated N-debenzoylated oxarbazole in urine. The profound changes in pharmacological activity that result from relatively small chemical modifications of the tetrahydrocarbazole nucleus make it likely that many further investigations of this class of compounds will be undertaken in the future.

Animals↗
PubMed1980

Disposition of trilostane in the rat and monkey.

The metabolism of trilostane, a novel inhibitor of adrenal steroidogenesis, was studied in the rat and monkey. In the rat, a peak blood level, equivalent to 2 microgram/ml of trilostane, was observed following a 25 mg/kg oral dose; excretion was mainly via the feces. In the monkey, the peak plasma level, equivalent to 15 microgram/ml, was observed 2 hr after a 20 mg/kg oral dose; elimination of radioactivity was predominantly in the urine. The five major metabolites of trilostane in monkey urine have been isolated and partially characterized. The primary metabolic pathways involved hydroxylation and glucuronide formation.

Androstanols↗