Search PubMed⌕ Search

Biomedical subjects

S A Stavchansky

Publications and source records attributed to S A Stavchansky.

4 recordsLinked to original sources
PubMed1979

Phenytoin cumulation kinetics.

Four male subjects were given phenytoin orally in single or twice-daily doses. Subjects were on 2 or 3 different dosing rates from 260 to 600 mg phenytoin sodium daily. Predose blood samples were obtained almost daily. The resulting serum levels, measured by gas-liquid chromatography, ranged from 1 to 18 micrograms/ml. Serum phenytoin concentration-time data were fit to a 1-compartment open model with zero-order input and Michaelis-Menten elimination. The resulting computer-generated parameter estimates (Vmax, 5.28 to 8.41 mg/kg/day; Km, 0.83 to 4.18 mg/1; Vd, 0.74 to 0.97 1/kg) are in agreement with the ranges of values in the literature. The time course of phenytoin cumulation is compatible with the presence of a major elimination pathway exhibiting Michaelis-Menten kinetic behavior.

Administration, Oral↗
PubMed1978

In vivo distribution of carbon-11 phenytoin and its major metabolite, and their use in scintigraphic imaging.

Curie quantities (0.3--1.5 Ci) of H11CN were used in the synthesis of C-11-tagged phenytoin (C-11.DPH) and 5-(p-hydroxyphenyl)-5-phenylhydantoin (C-11.HPPH), using a modified Bücherer-Bergs reaction. The H11CN was produced from a mixture of 95% nitrogen and 5% hydrogen by a 45-min bombardment with 10-MeV protons at 10 muA. Following i.v. infusions of C-11 DPH (13.7 mg/kg at a rate of 29 mg/min) into the left femoral vein of Rhesus monkeys, DPH shows persistent concentration in the brain and liver fields. Extravascular administration shows significant retention at the site of administration. Intravenous bolus injection of [11C]-HPPH into a Rhesus monkey, at a dose of 6.4 mg/kg, resulted in localization of this compound in the liver, gallbladder, urinary bladder, and intestinal fields. Loss of activity from the liver region, with appearance of this activity in the intestinal field, suggests that [11C]-HPPH is secreted into the intestine via the bile. Further investigation is needed to study the potential of [11C]-DPH as a brain-scanning agent and [11C]-HPPH as a possible cholescintigraphic agent.

Animals↗
PubMedDate not supplied

Kinetic and spectral studies of type I and type II compounds with rat hepatic microsomes in the presence of the major metabolite of diphenylhydantoin.

The nature of the inhibitory effects of the major metabolite of diphenylhydantoin, 5-(p-hydroxyphenyl)-5-phenylhydantoin (HPPH), on the in vitro metabolism of ethylmorphine and aniline by rat hepatic microsomes was examined. The N-demethylation of ethylmorphine was competitively inhibited by HPPH, whereas inhibition of the hydroxylation of aniline was not competitive. The spectrum produced by HPPH when added to microsomal suspensions does not resemble the classical type I or type II spectra, but rather a reversed type I spectrum. Spectral evidence is presented indicating that HPPH also diminishes the magnitude of the spectral change produced by type I and II compounds.

Aniline Compounds↗