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Biomedical subjects

J G Page

Publications and source records attributed to J G Page.

At least 37 records · Page 2Linked to original sources
PubMed1981

Treatment of the irritable bowel syndrome with Bentyl (dicyclomine hydrochloride).

The effectiveness of Bentyl (dicyclomine hydrochloride) 40 mg 4 times daily was evaluated in an ambulatory population with recent irritable bowel syndrome (IBS). During the 2-week double-blind study, the effects of dicyclomine hydrochloride compared to placebo were assesed by: 1) physicians' global evaluation of treatment, 2) patients' self-evaluation of treatment, and 3) patients' evaluation of duration of abdominal pain. It was concluded that over a 2-week period dicyclomine hydrochloride 40 mg 4 times a day is superior to placebo in improving the overall condition of the patient, decreasing abdominal pain, decreasing abdominal tenderness, and improving bowel habits. The majority of adverse effects reported were related to the anti-cholinergic activity of the drug.

Abdomen↗
PubMed1976

Metabolism of 1,4-dihydro-6-trifluoromethylquinoxaline-2,3-dione (Lilly 72525) in rats and cats.

1. The metabolism of 1,4-dihydro-6-trifluoromethylquinoxaline-2,3-dione (Lilly 72525), a sedative hypnotic drug, was studied in rat and cat. 2. Plasma concentrations of Lilly 72525 were measured fluorometrically after oral and intravenous doses of the compound in rats. A comparison of the area under the two curves suggested that 84% of the oral dose was absorbed. 3. Studies with 14C-labelled material in both species confirmed that the drug was well absorbed after oral administration and revealed that the dione was mainly eliminated unchanged in the urine. Bile duct cannulation experiments suggested that biliary excretion accounted for most or all of the drug present in faeces of rats. 4. Metabolites isolated from urinary extracts by t.l.c. were identified by g.l.c.-mass spectrometry. The only metabolite detected in rat urine or bile extracts was a ring-hydroxylated compound. This metabolite plus two N-hydroxylated metabolites were identified in extracts of cat urine.

Administration, Oral↗
PubMed1975

Species differences in the metabolism of alpha-1-trans-4-dimethylaminotetrahydro-3-furyl-cyclohexanephenylglycolate, an experimental anticholinergic agent.

Metabolism studies in the rat, dog and cat have demonstrated a definite species difference in biotransformation and elimination of alpha-1-trans-4-dimethylaminotetrahydro-3-furylcyclohexanephenylglycolate (Lilly 82537), an experimental anticholinergic agent. Separation and identification of urinary and biliary metabolites by gas chromatographic mass spectrometric analysis has shown three mechanisms to be involved in the metabolism of Lilly 82537 in these species; N-demethylation, aliphatic hydroxylation ahd ester hydrolysis. A major portion of the drug administered was eliminated unaltered in the cat and dog, while only trace quantities of parent drug were observed in the urine and bile of rats. These metabolic differences may be responsible for observed species differences in the pharmacologic activity of Lilly 82537.

Animals↗
PubMed1969

Genetic control of the phenobarbital-induced shortening of plasma antipyrine half-lives in man.

The mean half-life of antipyrine in the plasma of four sets of identical and four sets of fraternal twins after a single oral dose of 16 mg/kg of antipyrine was 12.7 +/-(SD) 3.3 hr. After 2 wk on sodium phenobarbital (2 mg/kg daily) the half-life of antipyrine in the plasma of these twins was reduced to 8.0 +/-(SD) 1.5 hr. Shortening of the plasma antipyrine half-life occurred in all but one of these 16 normal, adult volunteers, but there was considerable variation in the extent of reduction which ranged from 0 to 69%. Phenobarbital administration decreased individual variations in antipyrine metabolism as indicated by the smaller standard deviation of the plasma antipyrine half-lives after phenobarbital than observed initially and by the narrowed range of variation in plasma antipyrine half-lives from 2.8-fold initially to 1.8-fold after phenobarbital. These results suggest that some inducing agents may be used to minimize individual variations in drug metabolism where such variations create therapeutic problems by exposing patients who slowly metabolize certain drugs to toxicity and other patients who rapidly metabolize some drugs to undertreatment. During the course of phenobarbital administration blood levels were determined. Phenobarbital blood levels correlated neither with the final values for plasma antipyrine half-lives nor with the per cent reduction in plasma antipyrine half-life produced by phenobarbital treatment. There was a direct relationship between initial antipyrine half-lives and the per cent shortening of antipyrine half-life produced by phenobarbital administration: the shorter the initial antipyrine half-life, the less the reduction caused by phenobarbital treatment. Larger intrapair variances in fraternal than in identical twins indicate genetic, rather than environmental, control of phenobarbital-induced alterations in plasma antipyrine half-life.

Adult↗
PubMed1968

Genetic control of drug levels in man: antipyrine.

Antipyrine was administered to identical or monozygotic twins and to fraternal or dizygotic twins. Individuals with identical genotypes (monozygotic twins) exhibited significantly less variability in antipyrine halflife than did genetically different individuals (dizygotic twins). Therefore variations in antipyrine metabolism appear to be determined genetically rather than environmentally. In the 36 twins tested, antipyrine half-lives varied between 5.1 and 16.7 hours. No significant correlation occurred between half-lives for phenylbutazone and antipyrine in the 28 twins who received both drugs.

Adult↗
PubMed1968

Genetic control of drug levels in man: phenylbutazone.

Phenylbutazone was administered to seven pairs of identical (monozygotic) twins and to seven pairs of fraternal (dizygotic) twins. Individual half-lives ranged from 1.2 to 7.3 days. Subjects with identical genotypes (monozygotic twins) exhibited very similar phenylbutazone half-lives; significantly greater differences in half-life occurred in dizygotic twins. The previously established large variations among individuals in phenylbutazone metabolism appear to be genetically, rather than environmentally, determined.

Adult↗