Biomedical subjects
Publications and source records attributed to W J O'Reilly.
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Rats, with and without bile duct ligation (BDL), were injected with hexobarbital (i.p. and i.v.) and blood concentrations measured as a function of time. Analysis of these curves using a single-compartment model showed that BDL altered hexobarbital pharmacokinetics in a manner dependent upon the duration of BDL and the route of administration of hexobarbital. Clearance from the blood and the rate constant for elimination (K) were reduced after 72-hour BDL but not after 12-hour BDL. The absorption of hexobarbital after intraperitoneal injection was slowed by 12- and 72- hour BDL. Seventy-two-hour BDL also increased the volume of distribution of hexobarbital but only when the drug was administered intraperitoneally. These data are consistent with previously reported data showing impairment of hepatic microsomal drug metabolism after 72-hour BDL, but not after 12-hour BDL. We also confirmed earlier speculations that BDL decreased the absorption of intraperitoneally-administered hexobarbital, although this does not appear to be a significant factor in prolonging hexobarbital sleeping time.
In children, the blood level of phenytoin was found to be significantly higher when 100 mg capsules rather than 100 mg tablets were administered. When, on the other hand, 30 mg capsules and tablets were compared; the situation was reversed; tablets produced significantly higher blood levels of phenytoin than did the capsules. The significance and possible explantation of these findings are discussed.
A cross-over study was conducted to compare the plasma phenytoin levels produced by different phenytoin preparations available in Australia. The preparations were found not to be equivalent, a liquid suspension product producing higher levels compared with capsule and tablet formulations. The clinical significance and possible explantation are discussed.
The pharmacokinetics of N1-acetylsulphamethoxazole and N4-acetylsulphamethoxazole in man are described. N1-Acetylsulphamethoxazole is deacetylated to sulphamethoxazole and acetylated to N4-acetylsulphamethoxazole. N4-Acetylsulphamethoxazole is excreted almost unchanged in the urine. The renal excretion rate is independent of the urine flow and urinary pH. N4-Acetylsulphonamides are less lipid soluble and more acidic than their corresponding parent sulphonamides.