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Biomedical subjects

J N Miceli

Publications and source records attributed to J N Miceli.

36 records · Page 2Linked to original sources
PubMed1980

Pharmacokinetics of severe theophylline intoxication managed by peritoneal dialysis.

In a patient severely poisoned with theophylline, saturation kinetics were demonstrated at serum concentrations > 35 micrograms/ml with subsequent conversion to first order kinetics (t 1/2 = 5.4 h). Peritoneal dialysis was used to enhance the drug's removal. The mean theophylline clearance was greater for dialysate (5.11 ml/min) than for urine (1.98 ml/min) or gastric fluid (0.32 ml/min). Urinary elimination occurred as a constant first order process (t 1/2 = 4.3 h). Peritoneal dialysis is a valuable early adjunct in the management of severe theophylline intoxication.

Child, Preschool↗
PubMed1979

Peritoneal dialysis of theophylline.

The use of peritoneal dialysis as an adjunct to management of theophylline intoxication is presented. Due to the nature of the case, detailed pharmacokinetic explanation was not possible. The data indicate that appreciable quantities of theophylline can be removed using peritoneal dialysis.

Humans↗
PubMed1979

Simultaneous measurements of acetaminophen and salicylate in plasma by liquid chromatography.

We describe a "highly-performance" liquid chromatographic method in which 8-chlorotheophylline is used as an internal standard to determine acetaminophen and salicylate simultaneously in plasma samples. Therapeutic as well as toxic concentrations can be determined on samples as small as 50 micro L, which makes the method particularly useful for determinations on samples from young children. The procedure requires a simple extraction of the drugs, and the chromatography is completed in 6 min.

Acetaminophen↗
PubMed1976

Failure of commercially prepared isoniazid diet to produce isoniazid serum concentrations in rhesus monkeys.

A comparison was made of serum isoniazid concentrations and the time course of isoniazid elimination in rhesus monkeys given the drug im, orally on sugar cubes, or in a commercially medicated diet. When the drug was administered orally on sugar cubes or im, peak serum concentrations were usually reached within 2 hr. A threefold individual variation in the rate of elimination was noted, and in most animals the serum concentration at 6 hr approached zero. Isoniazid was not detected in the serum of any animal receiving the commercially medicated diet. Others using this medicated food in their tuberculosis prophylaxis programs should be aware that the diet probably does not provide therapeutically effective dosage to the animals.

Administration, Oral↗
PubMedDate not supplied

An improved method for the quantitation of phencyclidine (PCP) in biological samples utilizing nitrogen-detection gas chromatography.

A simplified method for the quantitation of phencyclidine using nitrogen-detection gas chromatography is described. The samples are extracted twice with n-butyl chloride containing benzphetamine as an internal standard. A 0.5 mL sample is required for detection of as little as 5 ng/mL PCP. The assay is easy, fast and reliable. Due to the relatively small volume required, this method is suitable for analysis of pediatric samples.

Child↗
PubMedDate not supplied

N-acetylation of drugs. Pharmacogenetic studies in rabbits selected for their acetylator characteristics.

Studies on acetylation of sulfadiazine, isoniazid, and p-aminobenzoic acid in selected lines of slow and rapid acetylator rabbits are described. Pedigree analysis of rabbits classified as slow or rapid sulfadiazine acetylators confirmed previous studies that the rate of sulfadiazine elimination (acetylation) is genetically controlled, with rapid elimination dominant over slow elimination of the drug. Pharmacokinetic studies in rabbits of specified sulfadiazine acetylator genotypes with isoniazid and p-aminobenzoic acid show that the rate of isoniazid elimination is under the same genetic control as is sulfadiazine, whereas the rate of p-aminobenzoic acid elimination is not. A new drug acetylation polymorphism, which controls the rate of enzymatic acetylation of p-aminobenzoic acid in peripheral blood cells and which is related to the sulfadiazine acetylation polymorphism, is described.

Acetyltransferases↗