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Biomedical subjects

H W Elliott

Publications and source records attributed to H W Elliott.

At least 19 recordsLinked to original sources
PubMed1977

Actions and metabolism of codeine (methylmorphine) administration by continuous intravenous infusion to humans.

Miosis produced by codeine is not antagonized by nalorphine until large oral doses are administered for several days. The present experiment was conducted in order to further study this characteristic of the codeine effect. Eight healthy male volunteers, who were former drug users, were divided into two groups. Subjects in the first group were given a continuous infusion of codeine, 30 mg/hr for 11-16 hr. No subjective effects were reported by the volunteers. In three of the individuals definite miosis antagonized by nalorphine was observed at 9.5 hr. The dose of codeine for the second group was 60 mg/hr for 11 hr. Mild but definite subjective effects were experienced by each of the participants in this group. Miosis appeared between 2 and 6 hr. Challenges at 4 and 6 hr were positive in two subjects and negative or equivocal in the other two. Codeine was excreted in the urine as free and conjugated codeine, morphine, and norcodeine. Maximum rates of excretion were similar for both groups, suggesting that the maximum amount of codeine that can be metabolized is equal or less than 30 mg/hr. Also codeine clearance, being greater than creatinine clearance, suggests that codeine might be excreted by glomerular filtration and tubular secretion. Blood levels of codeine in the 60 mg/hr group were about 10 times those reported as therapeutic. However, morphine or norcodeine were not detectable by the methods used.

Adult↗
PubMed1976

A comparison of the effect of propylthiouracil on the respiration of thyroid slices from humans, chickens and rats.

1. The QO2 of thyroid slices from hyperthyroid patients treated with propylthiouracil (PTU) was 140% that of slices from euthyroid patients. Similar results were obtained using thyroid slices from PTU fed and control chickens. 2. PTU feeding caused thyroid hyperplasia, increased QO2 more than could be accounted for by the hyperplasia but neither increased QO2 of muscle, cerebral cortex or spleen nor altered serum T4 levels. 3. PTU in drinking water increased the size and vascularity of thyroids from control but not hypophysectomized rats and had no effect on QO2. 4. The observations made on human, chicken and rat thryoid apparently reflect the effects of TSH rather than a direct action of PTU.

Adolescent↗
PubMed1976

Metabolism of lorazepam.

The metabolism of lorazepam by man and four other species is reviewed. Lorazepam and its metabolites in blood, urine and faeces were identified by thin-layer and gas chromatography and by mass spectrometry. The principal metabolite in man, dog, pig and cat is the glucuronide, but the rat produces other metabolites after small doses of lorazepam, and significant amounts of the glucuronide only after high doses. Since all metabolites, except the glucuronide, occur in small quantities only in man, most studies in man have been confined to an estimation of gree and conjugated lorazepam. Blood concentrations of unconjugated lorazepam peak at 1-4 h, significant concentrations persisting for 24 h and decreasing slowly over the next 24 h. About 95% of a dose of lorazepam was accounted for in urine and faeces over a period of 5 days; 74.5% was excreted in the urine as lorazepam glucuronide and 13.5% as minor metabolites. The excretory half-life was 12 h. The blood concentrations and excretion rates are compatible with the clinical effects of lorazepam.

Animals↗
PubMed1976

A comparative study of the analgesic and respiratory effects of N-allylnorcodeine (nalodeine), nalorphine, codeine and morphine.

In this comparative study, the abdominal constriction test was used to determine analgesia in mice, and the body plethysmograph was used to study respiratory effects of nalodeine, nalorphine, naloxone, codeine, morphine and various agonist-antagonist combinations in rats. The analgesia dose-response curves for the surrogate pairs, nalodeine-nalorphine and codeine-morphine, were parallel but had significantly different slopes. Naloxone was a more potent antagonist of morphine and codeine than of nalorphine and nalodeine. In antagonizing morphine and codeine analgesia, naloxone was the most potent antagonist, nalorphine had a biphasic effect with decreasing activity at higher doses and nalodeine was not an antagonist. Moderate doses of nalorphrine depressed minute volume largely by their effect on tidal volume, but high doses stimulated respiratory rate and therefore had less effect on minute volume. Nalodeine depressed minute volume by depressing tidal volume, since all doses initially stimulated and then variably affected respiratory rate. Metabolic rate was not increased by either drug short of convulsant doses. Nalodeine depresses the ventilatory response to CO2 and weakly antagonizes the respiratory depressant actions of morphine.

Analgesics↗
PubMed1975

Effects of street drugs on anesthesia.

The magnitude of the drug abuse problem in the United States and the pharmacological and toxicological actions of street drugs are discussed. The interactions of these drugs with anesthetics and related drugs and with the anesthetist and members of the health care team involved in pre- and post-operative care are pointed out, and methods of dealing with various problems are suggested.

Amphetamines↗