Year 2001 - Volume 21, Number 3


Title
Clinical and pathological aspects of experimental poisoning by sodium selenite in horses, 21(3):109-116
Authors

Abstract
ABSTRACT.- Néspoli P.B., Duarte M.D., Bezerra Jr P.S., Döbereiner J. & Peixoto P.V. 2001.[Clinical and pathological aspects of experimental poisoning by sodium selenite in horses] Aspectos clínico-patológicos da intoxicação experimental por selenito de sódio em eqüinos. Pesquisa Veterinária Brasileira 21(3):109-116. Depto Clínica Médica Veterinária, Universidade Federal de Mato Grosso, Av. Fernando Correa s/nº, Cuiabá, MT 78065-200, Brazil. E-mail: peixotop@ufrrj.br


Due to the numerous contradictions on selenium poisoining, and in arder to improve knowledge about the clinical, pathological and toxicological aspects, experiments were performed with intramuscular injections of sodium selenite in 9 horses. Peracute, acute, subacute and chronic poisoning was reproduced; some nervous symptoms observed in acute cases were similar to those described for "blind staggers". In spite of this, the conflicting and dubious feature of this formerly described disease tums very difficult any comparison. On the other hand, the chronic poisoning was the first experimental reproduction of "alkali disease" by the parenteral route in horses. When administered as one injection, the lethal dose for sodium selenite was 1.49 mg/kg. Various clinical and pathological observations regarding the cardiovascular and nervous system, not previously mentioned in the literature for horses, are described. There have to be mentioned especially, (1) as to clinical aspects, cardiac murmurs, arrythmia, splitting of the heart sounds and convulsions, (2) regarding post-mortem findings, flattening of the cerebral gyri and increase of the liquor, and (3) conceming histopathology, lysis and necrosis of neurons in the cortex, oedema of astrocytes, as well as activation of endothelial and glia cells. It is suggested, that the degenerative-necrotic alterations in the central nervous system could be due to the oedema caused by an increase in vascular permeability through the action of the selenite.
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