Submitted by Sandra Pereira (srpereira@ufrrj.br) on 2016-09-19T11:49:34Z No. of bitstreams: 1 2011 - Michel Jos? Sales A. Helayel.pdf: 11350186 bytes, checksum: ab1a4bf6f150ee6e971e58207f995bff (MD5) / Made available in DSpace on 2016-09-19T11:49:34Z (GMT). No. of bitstreams: 1 2011 - Michel Jos? Sales A. Helayel.pdf: 11350186 bytes, checksum: ab1a4bf6f150ee6e971e58207f995bff (MD5) Previous issue date: 2011-03-16 / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior - CAPES / This study aimed to evaluate the protective effect of acetamid in experimental poisoning by Pseudocalymma elegans in sheep, goats and rabbits, in order to prove indirectly that monofluoroacetate (MF) is responsible for the clinical signs and death of animals that ingested the plant. Experiments were performed to determine for sheep and goats the lethal dose of P. elegans collected in Rio Bonito, RJ, in different seasons, and to adjust the dose of acetamid to be administered. In the first experiment, four animals received 1.0g/kg of fresh P. elegans, and two others were pretreated with 2.0g/kg of acetamid. None of the animals showed clinical signs or died. Possibly, the plant could be less toxic, since it was collected at the end of the rainy season. In the second experiment, two sheep and two goats received 0.67 and 1.0g/kg of the dried plant, after pretreatment with 2.0 and 3.0g/kg of acetamid, respectively. All animals died, as the administered doses of P. elegans were very high. In the third experiment, two sheep and two goats received 0.333g/kg of dried P. elegans after previous administration of 2.0g/kg of acetamid; a week later, the protocol above was repeated, but without the antidote. In experiments with rabbits, doses of 0.5 and 1.0g/kg of dried P. elegans were given after administration of 3.0g/kg of acetamid; seven days later, the same protocol was repeated, except the administration of acetamide. This procedure, when acetamid was administered before, prevented the appearance of clinical signs and death of sheep, goats and rabbits. But the animals not treated with acetamid showed symptoms of poisoning and died. Clinically, the sheep and goats had tachycardia, engorged jugular vein, positive venous pulse, lateral recumbence, and muscle tremors. In the "dramatic phase?, the animals fell into lateral position, stretched the limbs, were paddling and died within minutes. The rabbits showed apathy, muscle tremors, vocalization and lateral decumbence minutes before death. At postmortem examination, the sheep and goats had engorged jugular veins and atria, dilated Vena cava cranialis and caudalis, as well as pulmonary edema, hepatic congestion and edema of the gallbladder subserosa. In rabbits, the main macroscopic alterations were dilated atria, engorged Vena cava cranialis and caudalis, and congested liver and diaphragm vessels. Histopathology revealed, in two sheep and one goat, vacuolar-hydropic degeneration of the distal convoluted kidney tubules, together with caryopicnosis. In the rabbits, the liver showed severe congestion with numerous shock corpuscles. The experimental results show indirectly that MF is to be held responsible for death of the animals that ingested P. elegans; since "acetate donor" compounds, such as acetamid, are capable to reduce the competitive inhibition of MF for the same active site (Coenzyme A) which prevents the formation of fluorocitrate, its active metabolite, formed in the body through the socalled "lethal synthesis". / O presente trabalho teve como objetivo avaliar o efeito protetor da acetamida nas intoxica??es experimentais por Pseudocalymma elegans (Bignoniaceae) em ovinos, caprinos e coelhos, com a finalidade de comprovar indiretamente que o monofluoroacetato ? respons?vel pela sintomatologia e morte dos animais que ingerem essa planta. Foram realizados experimentos para determinar a dose letal da planta coletada em Rio Bonito, RJ, em diferentes ?pocas do ano para ovinos e caprinos e ajustar a dose de acetamida a ser administrada. No primeiro experimento, dois ovinos e dois caprinos receberam 1,0 g/kg de P. elegans fresca e um animal de cada esp?cie foi tratado previamente com 2,0 g/kg de acetamida. Nenhum animal apresentou altera??es cl?nicas ou morreu. Ao que tudo indica a planta poderia estar menos t?xica, j? que foi coletada no fim da esta??o das ?guas. No segundo experimento, dois ovinos e dois caprinos receberam 0,67 e 1,0 g/kg da planta dessecada, ap?s tratamento pr?vio, com 2,0 e 3,0 g/kg de acetamida, respectivamente. Todos os animais morreram, pois administramos doses muito altas de P. elegans. No terceiro experimento, dois ovinos e dois caprinos receberam, 0,333 g/kg de P. elegans dessecada, ap?s administra??o pr?via de 2,0 g/kg de acetamida. Uma semana depois, o protocolo acima foi repetido, por?m sem o ant?doto. Nos experimentos com coelhos, foram administradas doses de 0,5 e 1,0 g/kg de P. elegans dessecada ap?s a administra??o de 3,0 g/kg de acetamida. Sete dias depois, o mesmo protocolo foi repetido, com exce??o da administra??o de acetamida. Esta, quando administrada previamente, evitou o aparecimento dos sinais cl?nicos e a morte dos ovinos, caprinos e coelhos, j? os animais n?o tratados com acetamida apresentaram sintomatologia e morreram. Clinicamente, os ovinos e caprinos manifestaram taquicardia, jugulares ingurgitadas, pulso venoso positivo, dec?bito esternal e tremores musculares. Na ?fase dram?tica?, os animais ca?am em dec?bito lateral, esticavam os membros, faziam movimentos de pedalagem e morriam em poucos minutos. Nos coelhos observaram-se apatia, tremores musculares, dec?bito lateral e vocaliza??o minutos antes da morte. A avalia??o macrosc?pica revelou, nos ovinos e caprinos, jugulares ingurgitadas, aur?culas, veia cava caudal e cranial dilatadas, al?m de edema pulmonar, congest?o hep?tica e edema na subserosa da ves?cula biliar. Nos coelhos as principais altera??es observadas foram aur?culas dilatadas, veia cava caudal e cranial ingurgitadas, f?gado e vasos do diafragma congestos. O exame histopatol?gico revelou, em dois ovinos e um caprino, degenera??o hidr?pico-vacuolar dos t?bulos urin?feros contornados distais associada ? cariopicnose. Nos coelhos havia congest?o hep?tica acentuada com numerosos corp?sculos de choque. Nossos resultados comprovam, de forma indireta, que o MF ? respons?vel pela morte dos animais que ingerem essa planta, uma vez que compostos ?doadores de acetato? como a acetamida, s?o capazes de reduzir a inibi??o competitiva do MF pelo mesmo s?tio ativo (Coenzima A), o que impede a forma??o do fluorocitrato, seu metab?lito ativo, formado no organismo por meio da denominada ?s?ntese letal?.