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Biomedical subjects

P R Martin

Publications and source records attributed to P R Martin.

5 recordsLinked to original sources
PubMed1979

Intravenous phenobarbital therapy in barbiturate and other hypnosedative withdrawal reactions: a kinetic approach.

Phenobarbital (0.03 to 0.04 mg/kg/min) was infused intravenously in 7 patients with clinical hypnosedative withdrawal reaction until patients slept but were arousable. The infusion time to reach this clinical end point was 7.8 +/- 1.1 hr (mean +/- SEM), the total dose was 992 +/- 144 mg, and the peak serum phenobarbital concentration was 26.1 +/- 5.1 micrograms/ml. A user of minimal hypnosedatives required 54% less phenobarbital and 65% lower concentration than any of the abusers to reach an equivalent state of intoxication. The mean serum half-life (t 1/2) was 57.5 +/- 4.9 hr for hypnosedative abusers and 86 +/- 3 hr for 8 normal volunteers (p less than 0.001). Only the patient with the shortest t 1/2 (36.4 hr) required oral phenobarbital supplements to prevent withdrawal symptoms. Dosage supplements required can be calculated from the postinfusion rate of fall of serum phenobarbital. Slow infusion of large amounts of phenobarbital provides a safe, efficacious single-dose treatment.

Adult↗
PubMed1978

Interaction of disulfiram with benzodiazepines.

The disposition of chlordiazepoxide (50 mg, intravenously), diazepam (0.143 mg/kg, orally), and oxazepam (0.429 mg/kg, orally) were studied in normal and alcoholic men before and after chronic disulfiram administration. Decreases in the plasma clearance of chlordiazepoxide (54%, p less than 0.05), diazepam (41%, p less than 0.05), and their active N-desmethyl metabolites were observed. Oxazepam has no important active metabolites and its net disposition is minimally altered by disulfiram. Oxazepam disposition is unaffected by age and liver disease. These considerations together with that of the short half-life of oxazepam (median, 6.1 hr) suggest that oxazepam may be the drug of choice if benzodiazepine therapy is used for patients taking disulfiram.

Adult↗
PubMed1976

Ribonucleic acid synthesis in the renal cortex at the initiation of compensatory growth.

The mechanisms responsible for the increase in RNA per cell during the first 48h of renal compensatory growth were studied in the renal cortex. Unilaterally nephrectomized, sham-operated or non-operated rats were used. Incorporation into RNA of labelled precursors was studied in vivo and in vitro. Sham-operation produced significant changes in precursor incorporation, absolute amounts of UTP and RNA, and the rate of RNA synthesis. At 6h after surgery, the amount of RNA decreased in sham-operated controls, whereas that in growing cortex remained unchanged. Incorporation into RNA in vivo was greater in the growing cortex, although the rate of RNA synthesis was not increased. At 24h, precursor incorporation into RNA and UTP and RNA synthesis were all increased in the growing cortex. In contrast with results obtained in vivo, slices of growing cortex incorporated less labelled precursor into RNA than did cortex slices from sham-operated controls, from 3 to 48h. Maximal differences were found from 6 to 24h. An attempt was made to equalize endogenous precursor pool sizes by increasing the concentration of unlabelled uridine in the media; incorporation differences were narrowed significantly. Serum from nephrectomized animals did not increase precursor incorporation into RNA in vitro. An increase in RNA synthesis is an important factor in RNA accretion in the renal cortex beyond 12h of compensatory growth. This is accompanied by increased UTP content and preceded by expansion of other pools. The amount of labelled precursor incorporated into RNA is greatly influenced by its delivery rate to the growing kidney in vivo and by intracellular dilution of expanded precursor pools in vitro.

Animals↗