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Biomedical subjects

J A Bogan

Publications and source records attributed to J A Bogan.

At least 55 records · Page 3Linked to original sources
PubMed1984

Effect of feeding on the fate of orally administered phenylbutazone, trimethoprim and sulphadiazine in the horse.

Phenylbutazone, sulphadiazine and trimethoprim were administered to three horses on two occasions, recently fed and unfed, and the effect of feeding on the pharmacokinetics of the three drugs assessed. The mean peak concentrations of phenylbutazone and trimethoprim were reduced by feeding by 34 and 75 per cent, respectively. The pharmacokinetics of sulphadiazine were not significantly affected.

Animals↗
PubMed1984

The binding and subsequent inhibition of tubulin polymerization in Ascaris suum (in vitro) by benzimidazole anthelmintics.

Benzimidazole anthelmintics may act by interfering with the microtubule system in Ascaris suum. Binding of benzimidazole anthelmintics, and their inactive metabolites, to A. suum tubulin was demonstrated by the inhibition of intestinal extracts of the nematode to bind [3H]colchicine. In addition, these compounds inhibited the polymerization of tubulin into microtubules in vitro.

Animals↗
PubMed1984

The fumarate reductase system as a site of anthelmintic attack in Ascaris suum.

Various benzimidazole compounds have been shown to be highly effective as inhibitors (up to 50% reduction of activity) in vitro of the helminth-specific enzyme, fumarate reductase, of Ascaris suum. Anthelmintically active and inactive benzimidazoles were similarly effective as inhibitors of enzyme activity. Albendazole-induced inhibition of fumarate reductase was not observed when the enzyme was preincubated with NADH.

Animals↗
PubMed1984

The pharmacokinetics of fenbendazole and oxfendazole in cattle.

The pharmacokinetics of fenbendazole and oxfendazole in cattle are described. The pharmacokinetics of oxfendazole were not significantly different when administered orally and by intra-ruminal injection. At a dose rate of 4.5 mg/kg, administered orally, fenbendazole gave rise to mean peak concentrations in plasma of fenbendazole and oxfendazole of 0.11 and 0.13 microgram/ml respectively. Oral administration of oxfendazole, at 4.5 mg/kg body weight, gave rise to plasma peak concentrations of fenbendazole and oxfendazole of 0.10 and 0.20 microgram/ml respectively. Following intra-ruminal administration of oxfendazole, the peak concentrations were 0.11 and 0.18 microgram/ml respectively.

Animals↗
PubMed1982

Pharmacological modulation of the pneumotoxicity of 3-methylindole.

The nature of the reactive metabolite of 3-methylindole is investigated using microsomal preparations prepared from the lungs of cattle. Nucleophilic thiol agents, glutathione, L-cysteine and N-acetyl-L-cysteine, protected microsomal proteins against alkylation by the reactive metabolite of 3-methylindole. The cytosol fraction from the lungs of cattle increased the protective effect of these thiol agents. Pretreatment of sheep with diethylmaleate, which depletes glutathione, increased the severity of the pneumotoxic effect of 3-methylindole, whereas pretreatment with L-cysteine decreased the severity of this effect. These findings are consistent with a hypothesis that an electrophilic reactive metabolite of 3-methylindole is responsible for its pneumotoxic effect and implies that glutathione and glutathione S-transferases are involved in the detoxification of this reactive metabolite. Nucleophilic thiol agents can be useful in the prevention of reactive metabolite induced-lung injury.

Animals↗
PubMed1982

Failure of 3-methylindole to contract the bovine pulmonary vein or to release mediators of anaphylaxis from the bovine lung in vitro.

Strips of smooth muscle from the pulmonary vein, pulmonary artery, trachea and bronchus of calves were incubated in an organ bath with 3-methylindole (3MI) and 3-methyloxindole (3MOI). 3MI and 3MOI (5-640 micrograms/ml) did not cause contraction of any of the isolated smooth muscle preparations. No evidence for the release of mediators of anaphylaxis was obtained when chopped bovine lung preparations were incubated with 3MI (20 micrograms/ml) and 3MOI (25 micrograms/ml). Results of the present work diminish the possibility that the pneumotoxic effect of 3MI is due to a primary hydrodynamic imbalance across the alveolocapillary membrane resulting in excess filtration over reabsorption.

Animals↗
PubMed1982

Pharmacokinetics of levamisole in sheep.

Levamisole, at a dose rate of 7.5 mg/kg, produced mean peak plasma concentrations of 3.1, 0.7 and 0.8 microgram/ml in four sheep after administrations by the subcutaneous, oral and intraruminal routes respectively. The mean peak concentrations in abomasal fluid were 33, 164 and 21 micrograms/ml respectively. The bioavailability of levamisole to the systemic compartment was less after oral and intraruminal administration than after subcutaneous administration. In six sheep there were no significant differences in the plasma concentrations obtained after subcutaneous administration in the thoracic, neck or gluteal regions. Dividing the dose between five sites in the gluteal region produced higher peak plasma concentrations than when injected into a single site.

Abomasum↗
PubMed1981

Lomotil in cats.

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Animals↗
PubMed1981

Pharmacokinetics of oxfendazole in sheep.

Pharmacokinetics of oxfendazole and its sulfone metabolite were determined in 6 sheep. Oxfendazole achieved mean peak plasma concentrations of 0.76 micrograms/ml at 30 hours after oral administration of oxfendazole (10 mg/kg of body weight), and concentrations were detectable for up to 7 days after administration. Mean peak abomasal concentrations of 3.55 micrograms/ml occurred 20 hours after administration and were detectable up to 9 days after administration. Concentrations of sulfone in plasma and abomasal fluid were generally lower than were those of oxfendazole.

Abomasum↗
PubMed1981

Pharmacokinetics of fenbendazole in sheep.

Concentrations of fenbendazole and its sulfoxide, oxfendazole, and sulfone metabolites were determined in 6 sheep after oral administration of fenbendazole (10 mg/kd of body weight). Mean peak concentrations in plasma of fenbendazole, oxfendazole, and sulfone of 0.15, 0.29, and 0.17 micrograms/ml occurred 24, 30, and 36 hours after administration, respectively. Mean peak concentrations in abomasal fluid were 1.82, 0.66, and 0.07 micrograms/ml occurring at 30, 48, and 72 hours, respectively. Fenbendazole and oxfendhzole were detectable in plasma and abomasal fluids for 5 days after administration. Much of the anthelmintic activity of fenbendazole may be due to the oxfendazole metabolite. Plasma concentrations of fenbendazole were less and persisted for a shorter period after intra-abomasal administration than after oral administration.

Abomasum↗
PubMed1980

Analysis of benzimidazoles in body fluids by high-performance liquid chromatography.

A simple assay for benzimidazole in plasma and GI fluids using high-performance liquid chromatography was developed. The benzimidazoles were extracted using ether and were chromatographed with methanol-ammonium carbonate mixtures as the eluting solvents. Benzimidazole was detectable in 4 ml of plasma or GI fluid to a limit of 20 ng/ml.

Animals↗