Pharmacokinetic Profile of Intravenous Liposomal Triamcinolone Acetonide in the Rabbit

Abraham, Isaac; Hilchie, J.C.; Mezei, Michael

doi:10.1002/jps.2600721212

Cited by 11 publications

(3 citation statements)

References 14 publications

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“…Other publications of the pharmacokinetics of TMC administered i.v. to humans and rabbits, reported that the pharmacokinetics of the drug were best described by a two-compartment open model (Abraham et al, 1983;Derendorf et al, 1995). This is in contrast to the three-compartment model that was appropriate for the behaviour of the steroid in horses.…”

Section: Discussionmentioning

confidence: 99%

Pharmacokinetics and metabolic effects of triamcinolone acetonide and their possible relationships to glucocorticoid-induced laminitis in horses

French

Pollitt

Pass

2000

J Vet Pharmacol Ther

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Experiments were performed to establish the pharmacokinetics of triamcinolone acetonide and the effects of the glucocorticoid on glucose metabolism in horses. The pharmacokinetics after intravenous (i.v.) dosing was best described by a three-compartment open model. There was rapid distribution from the central compartment followed by two phases of elimination. The half-life of the rapid elimination phase was 83.5 min and of the slower phase was 12 h. The term (Vss/Vc)-1was 12.3 indicating extensive distribution into the tissues. Triamcinolone acetonide given i.v. or intramuscularly (i.m. ) induced a prolonged period of hyperglycaemia, hyperinsulinaemia and hypertriglyceridaemia. Significant changes in plasma glucagon and serum non-esterified fatty acids were not observed. These observations suggest that the hyperglycaemia was a result of decreased glucose utilization by tissues and increased gluconeogenesis. The effects on glucose metabolism persisted for 3-4 days after triamcinolone was given i.m. at 0.05 mg/kg, the upper limit of the recommended dose range, and for 8 days when given at 0. 2 mg/kg. These observations, together with recent evidence implicating inhibition of glucose metabolism in the pathogenesis of equine laminitis, indicated that triamcinolone-induced laminitis may be associated with the long duration of action of the glucocorticoid when higher than recommended doses or when repeated doses are given.

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Section: Discussionmentioning

confidence: 99%

Pharmacokinetics and metabolic effects of triamcinolone acetonide and their possible relationships to glucocorticoid-induced laminitis in horses

French

Pollitt

Pass

2000

J Vet Pharmacol Ther

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show abstract

“…Other publications of the pharmacokinetics of TMC administered i.v. to humans and rabbits, reported that the pharmacokinetics of the drug were best described by a two‐compartment open model (Abraham et al , 1983; Derendorf et al , 1995). This is in contrast to the three‐compartment model that was appropriate for the behaviour of the steroid in horses.…”

Section: Discussionmentioning

confidence: 99%

Pharmacokinetics and metabolic effects of triamcinolone acetonide and their possible relationships to glucocorticoid‐induced laminitis in horses

French

Pollitt

Pass

2000

Vet Pharm & Therapeutics

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Pass, M. A. Pharmacokinetics and metabolic effects of triamcinolone acetonide and their possible relationships to glucocorticoid-induced laminitis in horses J. vet. Pharmacol. Therap. 23,[287][288][289][290][291][292] Experiments were performed to establish the pharmacokinetics of triamcinolone acetonide and the effects of the glucocorticoid on glucose metabolism in horses. The pharmacokinetics after intravenous (i.v.) dosing was best described by a three-compartment open model. There was rapid distribution from the central compartment followed by two phases of elimination. The half-life of the rapid elimination phase was 83.5 min and of the slower phase was 12 h. The term (V ss /V c )− 1was 12.3 indicating extensive distribution into the tissues. Triamcinolone acetonide given i.v. or intramuscularly (i.m.) induced a prolonged period of hyperglycaemia, hyperinsulinaemia and hypertriglyceridaemia. Significant changes in plasma glucagon and serum non-esterified fatty acids were not observed. These observations suggest that the hyperglycaemia was a result of decreased glucose utilization by tissues and increased gluconeogenesis. The effects on glucose metabolism persisted for 3 -4 days after triamcinolone was given i.m. at 0.05 mg/kg, the upper limit of the recommended dose range, and for 8 days when given at 0.2 mg/kg. These observations, together with recent evidence implicating inhibition of glucose metabolism in the pathogenesis of equine laminitis, indicated that triamcinolone-induced laminitis may be associated with the long duration of action of the glucocorticoid when higher than recommended doses or when repeated doses are given.

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“…16 ARer oral administration, the absolute bioavailability of vincamine in solution was poor (22 f 1%), while the absolute bioavailability of vincamine administered as a nanoparticle suspension was larger (36 k 2%), leading to a relative bioavailability of 162 5 20%. The absorption rate of vincamine, as reflected by peak-time values (Table 111, seemed to be faster with the nanoparticle suspension.…”

Section: Parametersmentioning

confidence: 99%

Disposition Kinetics and Oral Bioavailability of Vincamine-Loaded Polyalkyl Cyanoacrylate Nanoparticles

Maincent

Verge

Sado

et al. 1986

Journal of Pharmaceutical Sciences

115

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Pharmacokinetic Profile of Intravenous Liposomal Triamcinolone Acetonide in the Rabbit

Cited by 11 publications

References 14 publications

Pharmacokinetics and metabolic effects of triamcinolone acetonide and their possible relationships to glucocorticoid-induced laminitis in horses

Pharmacokinetics and metabolic effects of triamcinolone acetonide and their possible relationships to glucocorticoid-induced laminitis in horses

Pharmacokinetics and metabolic effects of triamcinolone acetonide and their possible relationships to glucocorticoid‐induced laminitis in horses

Disposition Kinetics and Oral Bioavailability of Vincamine-Loaded Polyalkyl Cyanoacrylate Nanoparticles

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