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Biomedical subjects

R M Welch

Publications and source records attributed to R M Welch.

99 records · Page 6Linked to original sources
PubMedDate not supplied

Nasal decongestant activity of pseudoephedrine.

The effectiveness of orally administered pseudoephedrine in patients with acute or chronic nonsuppurative rhinitis was evaluated under double-blind conditions. Intranasally administered ephedrine which was given to all patients at the end of this study served as the positive control. Marked nasal decongestant effects of a single oral dose of pseudoephedrine (60 mg tablet), as determined by a modified passive anterior, rhinometric technique occurred within 30 minutes and were maintained for at least four hours. The mean nasal decongestant response (delta % of baseline) of 57.2% was associated with a mean peak, plasma pseudoephedrine level of 274 ng/ml. In addition, the maximum response to oral pseudoephedrine treatment was equivalent to the response produced by ephedrine nasal spray. These results suggest that pseudoephedrine is an orally, effective nasal decongestant.

Acute Disease↗
PubMedDate not supplied

Pharmacokinetics and O-dealkylation of morphine-3-alkyl ethers in the rat. A radioimmunoassay study.

Radioimmunoassay procedures were used to investigate the relationship between the chemical structure and disposition of morphine, codeine, ethylmorphine, t-butylmorphine, and pholcodine. Male Sprague-Dawley rats received po or iv doses of each drug equivalent to 10 mg/kg free base. Blood samples were collected at various times over the 6-hr period after each drug administration, and plasma concentrations of the parent drugs and metabolically produced morphine were determined. A single ethylmorphine antiserum was used for analysis of codeine, ethylmorphine, t-butylmorphine, and pholcodine in separate experiments, whereas a specific morphine antiserum was used in the radioimmunoassay of this compound. The absolute oral bioavailabilities of morphine, codeine, ethylmorphine, and t-butylmorphine all were below 10%, whereas that of pholcodine was over 40%. Terminal half-lives of morphine, codeine, ethylmorphine, and t-butylmorphine after iv administration all were less than 45 min, while that of pholcoline was over 2 hr. Codeine, ethylmorphine, t-butylmorphine, and pholcodine did not appear to undergo conjugation, as evidenced by the similarity between areas under the curve for total (unconjugated plus conjugated) and parent (unconjugated) drugs. Amounts of metabolically produced morphine in rats treated with codeine, ethylmorphine, t-butylmorphine, or pholcodine differed markedly. After oral administration, presystemic O-dealkylation of codeine and ethylmorphine was much greater than that of t-butylmorphine or pholcodine, presumably due to the presence of much bulkier 3-alkyl substituents in the latter compounds. Thus, the ratio of the morphine AUC to that of parent drug after po administration was 1.37 for codeine and 1.60 for ethylmorphine, but only 0.08 for t-butylmorphine and 0.01 for pholcodine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Effect of 3-methylcholanthrene pretreatment on the bioavailability of phenacetin in the rat.

A thin-layer chromatographic procedure is described for the quantitative determination of phenacetin and acetaminophen in rat plasma. The method was used to determine the effect of 3-methylcholanthrene (3-MC) on the disposition and bioavailability of phenacetin following its oral and iv administration to rats. Pretreatment with 3-MC decreased the plasma half-life of phenacetin, after iv administration, from 28 min to 4.5 min and reduced the systemic bioavailability of phenacetin, after oral administration, from 45% in control rats to 6% in 3-MC-treated rats. By comparing the plasma levels of phenacetin in the portal circulation with those in the peripheral circulation, following the oral administration of phenacetin, it was concluded that the 7-fold reduction in the bioavailability of phenacetin observed in 3-MC treated rats was caused by a marked increase in the metabolism of phenacetin during its first pass through the liver.

Acetaminophen↗