Calcium gluconate and sodium succinate for therapy of sodium fluoroacetate experimental intoxication in cats: clinical and electrocardiographic evaluation

Sodium fluoroacetate (SFAC) or Compound 1080 is a potent rodenticide, largely used after 1946 for rodent and home pest control. The toxic effects of SFAC are caused by fluorocitrate action, a toxic metabolite, which has a competitive action with aconitase enzyme, leading to citrate accumulation and resulting in interference in energy production by Krebs cycle blockade. In the present study, domestic cats were intoxicated with oral doses of fluoroacetate (0.45 mg/kg). The intoxicated animals presented emesis, diarrhea with abdominal pain posture and an abdominal palpation, tachypnea, bilateral midriasis, hypothermia, hyperexcitability and convulsions. Blood gas analysis indicated decreased pH and bicarbonate levels. Serum ionized calcium was also decreased. ECG showed non-specific changes in ventricular repolarization and ventricular arrhythmias. The survival rate was 75% in the treated group with calcium gluconate and sodium succinate and 37.5% in the non-treated group.

Hematological and biochemical profiles and histopathological evaluation of experimental intoxication by sodium fluoroacetate in cats

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Effects of experimental amitraz intoxication in cats

Este trabalho estudou os efeitos da intoxicação experimental por amitraz em 16 gatos, distribuídos, aleatoriamente, em dois grupos: grupo amitraz - animais receberam amitraz a 1,5% na dose de 1,0 mg/kg IV; e grupo controle - animais sem amitraz. Parâmetros fisiológicos sangüíneos, do sistema cardiorespiratório e de sedação foram aferidos até 360min. Perfil sangüíneo, uréia, creatinina, alanina aminotransferase e aspartato aminotransferase não foram afetados pelo amitraz. Sedação, perda de reflexos, hipotermia, bradicardia, bradiarritmias, hipotensão, bradipnéia, midríase, além de transitória hiperglicemia, hipoinsulinemia e diminuição dos níveis de cortisol, foram observados nos gatos experimentalmente expostos ao amitraz. Os efeitos alfa 2-adrenérgicos induzidos pela intoxicação por amitraz em gatos são muito similares aos mesmos efeitos relatados em outras espécies, contribuindo com mais informações dessa intoxicação para a toxicologia veterinária.

Experimental poisoning by Senecio brasiliensis in calves: quantitative and semi-quantitative study on changes in the hepatic extracellular matrix and sinusoidal cells

A matriz extracelular (MEC) desempenha um papel importante em lesões hepáticas crônicas e tem sido estudada em modelos de intoxicação experimental. em bovinos, no entanto, não há estudos específicos sobre a MEC hepática normal ou com lesões crônicas. Por isso, foi desenvolvido um modelo de intoxicação experimental hepático usando Senecio brasilliensis, uma planta que contém alcalóides pirrolizidínicos e causa lesão hepática dependente da dose. Cinco bezerros receberam por via oral, 0.38g/kg de folhas secas por 24 dias. Biópsias hepáticas foram obtidas a cada 15 dias durante 60 dias. Sinais clínicos de complicações digestivas surgiram da terceira semana do experimento. Um bezerro morreu aos 45 dias e os outros quatro foram avaliados até os 60 dias. As biópsias hepáticas foram processadas para microscopia óptica, imuno-histoquímica e microscopia eletrônica de transmissão. No trigésimo dia, as lesões hepáticas eram progessivas caracterizadas por vacuolização hepatocelular, necrose, apoptose, megalocitose, e fibrose centrolobular, pericelular e portal. Foram realizadas avaliações quantitativas e semi-quantitativas de componentes da MEC hepática antes e após o aparecimento das lesões. Foi realizada morfometria do colágeno total e do sistema de fibras elásticas. Colágeno total e colágenos tipos I e III aumentaram progressivamente em todos os locais do fígado. Mudanças na localização, quantidade e disposição do sistema de fibras elásticas foram também observadas. Houve um aumento significativo de células de Kupffer aos 30 dias e de células sinusoidais totais aos 45 e 60 dias. As lesões hepáticas neste experimento foram progressivas mesmo após a remoção da planta. Lesões de fibrose severa foram localizadas principalmente nos espaços porta, seguido por fibrose veno-oclusiva e pericelular. Os colágenos tipo I e tipo III foram observados no fígado normal e no fígado dos bezerros afetados, com predomínio do tipo I. Nos bezerros afetados o aumento do colágeno total e do sistema de fibras elásticas foi paralelo ao aumento no número das células sinusoidais.

Intoxicação experimental de bovinos com toxina botulínica tipo D

Realizou-se uma intoxicação experimental em bovinos, pela administração oral, com diferentes doses de toxina botulínica tipo D. O objetivo foi determinar o tempo de permanência da toxina no sangue circulante de bovinos, pela detecção da toxina no soro mediante bioensaio em camundongos, e de verificar a presença da toxina no fígado, no baço, nos rins e no coração, e no conteúdo ruminal de bovinos que morreram e/ou foram sacrificados. Utilizaram-se 12 bovinos, mestiços, divididos em quatro grupos de três animais cada. Os grupos I, II e III receberam 200DL50/ml, 21.300DL50/ml e 63.200DL50/ml de toxina botulínica, respectivamente, e o grupo IV manteve-se como controle. A toxina foi detectada principalmente no soro dos bovinos pertencentes aos grupos II e III que receberam altas doses do inóculo tóxico, nos quais a toxina permaneceu por um período de um a sete dias após o aparecimento dos primeiros sinais clínicos da doença. A toxina não foi detectada no fígado, no baço, nos rins e no coração, mas o foi no conteúdo ruminal de um bovino do grupo II. A toxina botulínica foi mais facilmente detectada no soro do que nos órgãos dos bovinos, sendo encontrada principalmente quando o animal ingeriu muita toxina, durante a fase inicial da doença e por um período de sete dias.

Estudo clínico e laboratorial da intoxicação experimental por amitraz em gatos e comparação entre ioimbina e atipamezole como tratamento

Pós-graduação em Medicina Veterinária - FMVZ

Quantificação de citocinas na intoxicação experimental com veneno de Crotalus durissus terrificus e Bothropoides jararaca em ratos Wistar tratados com soroterapia e Mikania glomerata

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Estudo dos aspectos clínico, laboratorial, histopatológico e do tratamento na intoxicação experimental pelo veneno da serpente Crotalus durissus terrificus em cães

Pós-graduação em Medicina Veterinária - FMVZ

Quantificação de citocinas no soro e homogenato da pata na intoxicação experimental com veneno de Bothropoides jararaca em ratos Wistar tratados com soroterapia e Mikania glomerata

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Hepatoprotective treatment attenuates oxidative damages induced by carbon tetrachloride in rats

The present study evaluated the hepatoprotective effect of an N-acetyl or-methionine + choline chloride + caffeine + thiamine hydrochloride + nicotinamide + pyridoxine hydrochloride compound at doses of 0.2, 0.6 and 1.0 mL/kg of b.w., and the assessment was done by the investigation of serum-enzymatic activity, metabolic functions of the liver and histophatological changes in female Wistar rats, which were subjected to experimental intoxication with CCl4. One hundred and nineteen rats were randomly distributed into 17 groups, performing five different treatments, being evaluated seven animals per treatment in four periods: 2, 4, 6 and 8 days after CCl4-induced intoxication. Treated rats with the hepatoprotective medicine (HM) presented a significant reduction in infiltration of inflammatory cells, steatosis, necrosis and liver congestion when compared to non-treated rats (control). Beside these results, the treatment showed a positive effect on circulatory alterations in the intoxicated animals, with reduction of spleen and renal congestion, as well as, promotion of a significant improvement in ALT, AST, LDH, ALP, GGT enzymatic serum activity reduction and in recovering liver function regarding the metabolism of urea, triglycerides and glucose. These findings indicate therapeutic usefulness of the compound when administered at dose 0.6 and 1.0 mL/kg of b.w. in female Wistar rats. (C) 2010 Elsevier GmbH. All rights reserved.

Evidências clínico-patológicas de ovinos intoxicados experimentalmente com sementes de Crotalaria spectabilis (Leg.papilionoidea)

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Lesões hepáticas de bovinos intoxicados experimentalmente por Senecio brasiliensis (Compositae): estudo semi-quantitativo e quantitativo da matriz extracelular e de células sinusoidais

Pós-graduação em Patologia - FMB

Species differences in acrylonitrile metabolism and toxicity between experimental animals and humans based on observations in human accidental poisonings

The high acute toxicity of acrylonitrile may be a result of its intrinsic biological reactivity or of its metabolite cyanide. Intravenous N-acetylcysteine has been recommended for treatment of accidental intoxications in acrylonitrile workers, but such recommendations vary internationally. Acrylonitrile is metabolized in humans and experimental animals via two competing pathways; the glutathione-dependent pathway is considered to represent an avenue of detoxication whilst the oxidative pathway leads to a genotoxic epoxide, cyanoethylene oxide, and to elimination of cyanide. Cases of acute acrylonitrile overexposure or intoxication have occurred within persons having industrial contact with acrylonitrile; the route of exposure was by inhalation and/or by skin contact. The combined observations lead to the conclusion of a much higher impact of the oxidative metabolism of acrylonitrile in humans than in rodents. This is confirmed by differences in the clinical picture of acute life-threatening intoxications in both species, as well as by differential efficacies of antidotes. A combination of N-acetylcysteine with sodium thiosulfate seems an appropriate measure for antidote therapy of acute acrylonitrile intoxications. Clinical observations also highlight the practical importance of human individual susceptibility differences. Furthermore, differential adduct monitoring, assessing protein adducts with different rates of decay, enables the development of more elaborated biological monitoring strategies for the surveillance of workers with potential acrylonitrile contact.

Biochemical Effect of Dicarboxylic Acids on Oxalate Metabolism in Experimental Rats and Studies on Oxalate Degrading Bacteria

The current study is an attempt to find a means of lowering oxalate concentration in individuals susceptible to recurrent calcium oxalate stone disease.The formation of renal stone composed of calcium oxalate is a complex process that remains poorly understood and treatment of idiopathic recurrent stone formers is quite difficult and this area has attracted lots of research workers. The main objective of this work are to study the effect of certain mono and dicarboxylic acids on calcium oxalate crystal growth in vitro, isolation and characterization of oxalate degrading bacteria, study the biochemical effect of sodium glycollate and dicarboxylic acids on oxalate metabolism in experimental stone forming rats and To investigate the effect of dicarboxylic acids on oxalate metabolism in experimental hyperoxaluric rats. Oxalic acid is one of the most highly oxidized organic compound widely distributed in the diets of man and animals, and ingestion of plants that contain high concentration of oxalate may lead to intoxication. Excessive ingestion of dietary oxalate may lead to hyperoxaluria and calcium oxalate stone disease.The formation of calcium oxalate stone in the urine is dependent on the saturation level of both calcium and oxalate. Thus the management of one or both of these ions in individuals susceptible to urolithiasis appears to be important. The control of endogenous oxalate synthesis from its precursors in hyperoxaluric situation is likely to yield beneficial results and can be a useful approach in the medical management of urinary stones. A variety of compounds have been investigated to curtain endogenous oxalate synthesis which is a crucial factor, most of these compounds have not proved to be effective in the in vivo situation and some of them are not free from the toxic effect. The non-operative management of stone disease has been practiced in ancient India in the three famous indigenous systems of medicine, Ayurveda, Unani and Siddha, and proved to be effective.However the efficiency of most of these substances is still questionable and demands further study. Man as well as other mammals cannot metabolize oxalic acid. Excessive ingestion of oxalic acid can arise from oxalate rich food and from its major metabolic precursors, glycollate, glyoxylate and ascorbic acid can lead to an acute oxalate toxicity. Increasedlevels of circulating oxalate, which can result in a variety of diseases including renal failure and oxalate lithiasis. The ability to enzymatically degrade oxalate to less noxious Isubstances, formate and CO2, could benefit a great number of individuals including those afflicted with hyperoxaluria and calcium oxalate stone disease.

Effects of calcium gluconate and PMSF in the treatment of acute intoxication of chicken by TOCP

To examine the efficacy of calcium gluconate (two doses of Ca-Glu 5 mg/kg i.v.) to alleviate the injurious effects of organophosphorus induced delayed neuropathy (OPIDN) in the presence or absence of phenylmethanesulfonyl fluoride (PMSF go mg/kg i.m.), 14 groups of four isabrown hens were used. To measure the lymphocyte neuropathy target esterase (LNTE)activity, groups receiving just distilled water (control), groups receiving just Tri-orto-cresyl phosphate (TOCP; 500 mg/kg p.o.) (Positive control), and other groups receiving TOCP and Ca-Glu or PMSF simultaneously or 12 hours later following intoxication by TOCP were used. They were sacrificed 12 and 24 hours after the administration of TOCP. To observe a 28-day time course of neurotoxicity scores and calcium plasma concentration, five groups were used. Regarding free Ca(2+)in the plasma, the positive control produced a characteristic profile time course up and down (luring 28 days, and some hens with maximum score of neurotoxicity in 28 days. The treatment, which prevented greater oscillation in free Ca(2+) in the plasma, presented a decrease in OPIDN in relation to the positive control. Twelve hours after the administration of TOCP, LNTE was 70-80% inhibited when compared with control, whereas the first decrease in the free Ca(2+) in the plasma was significantly different from the control only 24 hours after the administration of TOCP. In summary, the sooner the Ca-Glu is started, the less severe the neuropathy effects.