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Houpt, T. R., & Houpt, K. A. (1971). Nitrogen conservation by ponies fed a low -protein ration. Am J Vet Res, 32(4), 579–588.
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Alexander, F. (1982). Effect of phenylbutazone on electrolyte metabolism in ponies. Vet. Rec., 110(12), 271–272.
Abstract: Phenylbutazone administered in therapeutic doses to ponies decreased urinary sodium and chloride excretion. The volume and osmolality of the urine was unaffected as was potassium excretion. Faecal excretion of chloride decreased and that of potassium increased, while faecal sodium excretion was unaffected. Plasma pH, bicarbonate and total carbon dioxide decreased after phenylbutazone administration. Packed cell volume, plasma sodium, potassium, carbon dioxide tension and chloride were unchanged.
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Alexander, F. (1978). The effect of some anti-diarrhoeal drugs on intestinal transit and faecal excretion of water and electrolytes in the horse. Equine Vet J, 10(4), 229–234.
Abstract: The effect of morphine, Tinct. opii, loperamide, pethidine and atropine on intestinal transit and the faecal and urinary excretion of water and electrolytes was studied in ponies. The rate of passage of a particulate marker was slowed by morphine, hastened then slowed by loperamide and Tinct. opii, and hastened by atropine. The liquid marker was slowed by Tinct. opii and hastened then slowed by the other drugs. Only loperamide decreased the faecal sodium excretion. This drug also decreased faecal water and weight; it appeared worthy of clinical trial in diarrhoea. Tinct. opii decreased by morphine, pethidine and atropine increased faecal water.
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Alexander, F., & Collett, R. A. (1974). Proceedings: Some observations on the pharmacokinetics of trimethoprim in the horse. Br J Pharmacol, 52(1), 142p.
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Alexander, F., & Collett, R. A. (1974). Pethidine in the horse. Res Vet Sci, 17(1), 136–137.
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Alexander, F., & Davies, M. E. (1969). Studies on vitamin B12 in the horse. Br. Vet. J., 125(4), 169–176.
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Weik, H., Lingk, W., & Altmann, H. J. (1972). [Behavior of individual fatty acids during in-vitro lipolysis and resynthesis in equine depot fat]. Zentralbl Veterinarmed A, 19(8), 677–685.
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Weik, H., & Altmann, H. J. (1971). [Behavior of blood lipids during fasting in the horse]. Zentralbl Veterinarmed A, 18(2), 131–138.
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Bottoms, G. D., Roesel, O. F., Rausch, F. D., & Akins, E. L. (1972). Circadian variation in plasma cortisol and corticosterone in pigs and mares. Am J Vet Res, 33(4), 785–790.
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Dirikolu, L., Lehner, A. F., Karpiesiuk, W., Hughes, C., Woods, W. E., Boyles, J., et al. (2003). Detection, quantification, metabolism, and behavioral effects of selegiline in horses. Vet Ther, 4(3), 257–268.
Abstract: Selegiline ([R]-[-]N,alpha-dimethyl-N-2- propynylphenethylamine or l-deprenyl), an irreversible inhibitor of monoamine oxidase, is a classic antidyskinetic and antiparkinsonian agent widely used in human medicine both as monotherapy and as an adjunct to levodopa therapy. Selegiline is classified by the Association of Racing Commissioners International (ARCI) as a class 2 agent, and is considered to have high abuse potential in racing horses. A highly sensitive LC/MS/MS quantitative analytical method has been developed for selegiline and its potential metabolites amphetamine and methamphetamine using commercially available deuterated analogs of these compounds as internal standards. After administering 40 mg of selegiline orally to two horses, relatively low (<60 ng/ml) concentrations of parent selegiline, amphetamine, and methamphetamine were recovered in urine samples. However, relatively high urinary concentrations of another selegiline metabolite were found, tentatively identified as N- desmethylselegiline. This metabolite was synthesized and found to be indistinguishable from the new metabolite recovered from horse urine, thereby confirming the chemical identity of the equine metabolite. Additionally, analysis of urine samples from four horses dosed with 50 mg of selegiline confirmed that N-desmethylselegiline is the major urinary metabolite of selegiline in horses. In related behavior studies, p.o. and i.v. administration of 30 mg of selegiline produced no significant changes in either locomotor activities or heart rates.
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