Suicide in veterinary medicine: A literature review.

Veterinarians are commonly exposed to occupational stressors, including excessive workload and financial constraints. These stressors can lead to psychological distress, which typically results in mental health disorders such as depression, anxiety, and burnout and can even culminate in suicide attempts or suicide deaths. Risk factors associated with poor mental health and high rates of suicide in veterinary practitioners include continuous exposure to challenging scenarios, such as interpersonal conflicts, performing euthanasia, and easy access to lethal means of suicide, such as opioids and anesthetics. The previous studies highlight the urgent need for a better understanding of predisposing factors, mental health-related improvements in the professional environment, and the subsequent establishment of primary mental health-related care policies. Effective ways to promote mental health and prevent suicide may include social support, resilience, developing coping skills, promoting a healthy work environment, and discouraging perfectionist behaviors. This review aimed to summarize findings in studies that have investigated mental health and suicide in veterinarians and veterinary students and highlight measures that could be implemented as options for mental health promotion and suicide prevention.

Effects of Sodium Monensin on Copper Metabolism of Brazilian Santa Inês Sheep Submitted to Different Dietary Copper.

This study aimed to evaluate the influence of sodium monensin on the hepatic accumulation of copper in sheep. Twenty-four Santa Inês crossbred sheep were used and allocated in a 2 × 2 factorial experiment with six repetitions and considering the factors dietary copper (basal and high) and supplementation (with and without sodium monensin). Thus, four homogeneous groups were formed: control (basal diet); monensin (Mon), 30 ppm of monensin; copper (Cu), 10 10 mg/kg BW per day of copper; monensin + copper (MonCu). The experimental period lasted 14 weeks. Liver and bile samples were collected at the beginning and end of the experiment to determine mineral element concentrations, and weekly blood samples for biochemical, hematological, and mineral evaluation. Liver copper concentrations at the beginning of the experiment did not vary between groups, while mean liver copper concentrations at the end of the experiment were higher in the MonCu, Cu, and Mon groups when compared to the control. At the end of the study, hepatic copper concentration was influenced by copper (p = 0.0001) and monensin (p = 0.0003) supplementation. Copper-supplemented groups had reduced liver iron contents (p = 0.0287) and increased copper concentrations in bile. The biochemical evaluation showed increased serum GGT and AST activity (p < 0.05) in the Cu and MonCu groups from the eleventh week on compared to the control and Mon groups. The increase in activity of these enzymes was influenced by copper supplementation (p = 0.0340). Monensin interferes positively with the hepatic accumulation of copper and the supplementation of this additive may predispose sheep to copper poisoning.

Metabolic Profile of Steers Subjected to Normal Feeding, Fasting, and Re-Feeding Conditions.

The effects of feeding, fasting, and re-feeding on the metabolic and ruminal profiles of growing cattle were studied. Blood and urine samples were obtained from 12 crossbred steers weighing approximately 300 kg during the following periods: 11 h of normal feeding (postprandial period), 48 consecutive hours of fasting, followed by 48 h of re-feeding. Compared with the postprandial period, fasting caused the following modifications: moderate hypoglycemia accompanied by remarkable lipolysis detected by the increase in plasma levels of free fatty acids (FFAs); absence of hepatic lipidosis, as there were no changes in aspartate aminotransferase activity or serum cholesterol levels; mild ketogenesis, confirmed by the slight increase of ß-hydroxybutyrate (ßHB); increased amino acid burn for energy production, verified by the increase in serum urea contents. There were strong positive correlations between the plasma levels of FFAs and ßHB (r = 0.68; p < 0.001), fasting duration and FFA concentration (r = 0.92; p < 0.00001), and fasting duration and serum urea (r = 0.52; p < 0.001); there was a negative correlation between fasting duration and blood glucose (r = -0.52; p < 0.0001). During this same period, mild hypovolemia characterized by an increase in intravascular volume deficit was observed. The metabolic condition observed during fasting was completely reversed during re-feeding, except for the temporarily higher proteolysis.

Dietary Zinc Supplementation to Prevent Chronic Copper Poisoning in Sheep.

The aim of this study was to evaluate whether zinc (Zn) supplementation protects against hepatic copper (Cu) accumulation in copper-loaded sheep. Forty cross-bred lambs were assigned to five experimental groups. These included the control group (C) and four treatment groups that received Cu and/or Zn supplementation (dry matter (DM) basis) over 14 weeks, as follows: Cu (450 mg Cu/kg); Zn-35 (450 mg Cu + 35 mg Zn/kg); Zn-150 (450 mg Cu + 150 mg Zn/kg); and Zn-300 (450 mg Cu + 300 mg Zn/kg). Blood, liver, and bile samples were obtained for mineral determination by inductively coupled plasma optical emission spectrometry (ICP⁻OES). The hepatic metallothionein (MT) concentrations were also determined. At the end of the experiment, hepatic Cu concentrations were higher in all Cu-supplemented groups than in C. Hepatic Cu accumulation was lower in the groups receiving the Zn supplementation than in the Cu group, although the difference was only statistically significant (66%) in the Zn-300 group. The MT concentrations tended to be higher (almost two-fold) in the Zn groups (but were not dose related) than in the C and Cu groups, and they were related to hepatic Zn concentrations. Zn supplementation at 300 mg/kg DM is useful for preventing excessive hepatic Cu accumulation in sheep exposed to high dietary concentrations of Cu.

Avaliação clínica do uso de solução salina hipertônica no tratamento da acidose láctica ruminal aguda em bovinos / Clinical evaluation of hypertonic saline solution treatment for acute ruminal lactic acidosis on cattle

A infusão de solução salina hipertônica (SSH) é um importante tratamento em animais com choque hipovolêmico. Bovinos com acidose láctica ruminal aguda (ALRA) frequentemente apresentam quadros de desidratação. Este trabalho avaliou a eficiência do tratamento da ALRA com SSH. Foram empregados 12 bovinos machos, mestiços com um ano de idade. Após implantação de cânula ruminal e período de adaptação alimentar os animais foram submetidos à indução de ALRA por meio de administração de sacarose no rúmen. Após 20 horas da indução, os animais foram aleatoriamente divididos em dois grupos. Um deles (SSH) foi tratado na 20ª h com 5 mL/kg P.V. de uma solução de SSH (7,5 % NaCl), dentro de 15 min, e em seguida 20 mL/kg/P.V. de solução salina isotônica (SSI), no decorrer dos próximos 165 minutos. O outro grupo (SSI) foi medicado da mesma forma, com exceção da SSH que foi substituído por 5 mL/kg PV de SSI. Cinco litros de conteúdo ruminal foram retirados, sendo repostos com cinco litros de água em ambos os grupos. Variáveis foram mensuradas no momento 0 (MO), na 20ª h (M20h) e no decorrer dos tratamentos (M30´, M60´, M120´ e M180´). O uso de SSH provocou, nos primeiros 30 minutos, uma ligeira acidemia, acompanhada de discreta hipercapnia, contudo sem provocar efeitos colaterais. A infusão de SSH provocou uma queda no volume globular, confirmando a migração de fluidos do rúmen para a circulação, corrigindo parcialmente a desidratação. Assim, o uso de SSH é uma possibilidade de tratamento adicional da desidratação provocada pela ALRA.

Hypertonic saline solution (HSS) is known as an important treatment for hypovolemic shock. Cattle with acute rumen lactic acidosis (ARLA) usually present different degrees of dehydration. This study evaluated the efficiency of HSS for treatment of ARLA. Twelve yearling, cross-bred, male cattle were used. After an adaptation period, when a rumen cannula was implanted, the animals were submitted to an induction of ARLA by the administration of sucrose into the rumen. Twenty hours later the cattle were randomly divided in two groups. The 1st group was treated with 5 mL/kg BW with 7.5 % (NaCl), within 15 min after 20th h of the induction; thereafter it was infused 20 mL/ kg BW of isotonic saline solution (ISS) for the next 165 min. The 2nd group was treated only with ISS. Five liters of ruminal contents were removed and replaced with five liters of water in both groups. Variables were measured at time 0 (MO), 20 h (M20h) and throughout the treatment (M30´, M60´, M120´ e M180´). The use of HSS caused a mild acidemia followed by a discrete hypercapnia. No side effects were seen in cattle treated with HSS. Infusion of HSS decreased the globular volume indicating a passage of fluids from the rumen into the bloodstream, correcting partially the dehydration. The use of HHS is a possible additional treatment for correction of dehydration caused by ARLA.

Avaliação laboratorial do uso de solução salina hipertônica e isotônica e de furosemida no tratamento da intoxicação por amônia em bovinos / Laboratorial evaluation of hypertonic and isotonic saline solution and furosemide use for the ammonia poisoning treatment in cattle

Para testar a eficiência de vários tratamentos de intoxicação por amônia em bovinos, foram utilizados 25 garrotes que receberam cloreto de amônio por infusão intravenosa (iv) até o surgimento de quadro convulsivo. Em seguida, os animais foram alocados em um dos cinco grupos experimentais e tratados da seguinte forma: 1) controle: infusão (iv) de 300mL de solução salina isotônica (SSI), no decorrer de 4h; 2) infusão (iv) de 30mL kg-1 PV de SSI no decorrer de 4h e administração de 4L de água intraruminal por meio de sonda esofágica (ASE); 3) mesmo tratamento do grupo 2 e dose única (iv) de furosemida (2mg kg-1 PV) (F); 4) injeção (iv) de 5mL kg-1 PV de solução salina hipertônica (SSH) 7,2 por cento nos primeiros 30min, seguida de 20mL kg-1 PV de SSI e 4L de ASE; 5) mesmo tratamento do grupo 4 e dose única de F. No decorrer de 4h após a convulsão, foram determinados os teores plasmáticos de amônia e glicose, ureia, creatinina, potássio e sódio séricos, volume e gravidade específica da urina, e excreção urinária de amônio e ureia. No momento da convulsão, os teores de amônia plasmáticos foram muito altos e idênticos em todos os tratamentos, mas no 120°min, nos grupos tratados com associação de SSH+SSI+ASE (grupos 4 e 5), houve diminuição desse metabólito. O uso de furosemida (grupos 3 e 5) não aumentou a excreção total de urina. A terapia com associação de SSH+SSI+ASE aumentou ainda o volume urinário e a excreção percentual urinária de ureia e amônia durante o período crítico da 1ª hora de tratamento, mas o uso de SSI+ASE (grupos 2 e 3) teve resultados intermediários. A eficiência do tratamento com SSH+SSI+ASE ou SSI+ASE foi superior ao grupo controle. Embora com efeito menor que o observado com SSH+SSI+ASE, a SSI+ASE promoveu melhora no quadro clínico geral e, ao término do experimento, promoveu também uma adequada desintoxicação da amônia.

To test the efficiency of some treatments for ammonia poisoning in cattle, 25 steers were used. Ammonium chloride solution was infused intravenously (iv) in each steer until the onset of convulsive episode. Thereafter, the animals were distributed in one of the five different groups, as follows: 1) control: infusion (iv) of 300mL isotonic saline solution (ISS) throughout the following 4h; 2) infusion (iv) of ISS 30mL kg-1 BW throughout the following 4h and administration of 4L water (W) through stomach tube; 3) the same as group 2, plus a single dose (iv) 2g furosemide kg-1 BW (F); 4) injection of 5mL kg-1 BW hypertonic saline solution (HSS) (7.2 percent) (iv) throughout the first 30min, followed by 20mL kg-1 BW of ISS and 4L W.; 5) the same as group 4 and a single dose of F. For the next 4h after the convulsion, plasma concentration of ammonia and glucose, serum urea, creatinine, sodium and potassium, urine total volume and specific gravity, and urinary excretion of ammonium and urea were followed. At the convulsion, the ammonia blood levels were high and similar among the groups, but at the 120th min the animals treated with HSS+ISS+W (groups 4 and 5) had lower values than the control. Furosemide (groups 3 and 5) did not prevent an increase in the total excretion of urine. The therapy with HSS+ISS+W still increased the urinary volume and the total urinary excretion of urea and ammonium during the critical 1st h of treatment, while the use of ISS+W had intermediate results. The efficiency of the treatment with HSS+ISS+W or ISS+W was better than the control group. Although with lower efficiency as seen in the treatment with HSS+ISS+W, the ISS+W caused an improvement in the clinical picture and at the end of the experiment generated an adequate ammonia detoxification.

Intoxicação por amônia em bovinos que receberam uréia extrusada ou granulada: alterações em alguns componentes bioquímicos do sangue / Ammonia poisoning in cattle fed extruded or prilled urea: alterations in some chemistry components

Doze garrotes Girolando nunca alimentados com uréia foram distribuídos em dois grupos de seis animais cada, e induzidos a desenvolver um quadro de intoxicação por amônia através da administração de uréia extrusada ou granulada em dose única (0,5 g/kg PV). Foram determinados no plasma ou soro os teores de amônia, glicose, L-lactato, uréia e creatinina, além do volume globular em sangue total nos seguintes momentos: antes da administração de uréia, no surgimento dos tremores, após o primeiro episódio convulsivo, e após 240 minutos do início do experimento. A hiperamoniemia ocorreu a partir dos primeiro tremores. Maiores glicemia e lactemia-L foram constatadas no momento do ápice da intoxicação (episódio convulsivo), os quais foram superiores ao tempo basal. A produção endógena de uréia aumentou no decorrer do experimento devido à hiperamoniemia (r = 0,57), atingindo seus valores mais altos ao término do experimento. Quanto maior foi o teor de amônia, maiores foram as concentrações de lactato-L, glicose, uréia, creatinina e volume globular. Estes resultados permitem concluir que o grau de hiperamoniemia aumentou a gliconeogênese, a glicólise anaeróbica, a síntese de uréia endógena e o grau de desidratação. Entre as variáveis estudadas os teores de glicose e de lactato-L foram os melhores indicadores para monitorar alterações bioquímicas na intoxicação pela amônia

Twelve yearling Girolando steers never fed urea before were assigned randomly in two groups of six animals each. In both groups were administered intraruminally a single dose (0.5 g/kg BW) of extruded or prilled urea in order to induce ammonia poisoning. Plasma or serum levels of ammonia, urea, creatinine, glucose, L-lactate were determined. Hematocrit values were also recorded. Blood samples were taken before the administration of urea, at the onset of muscle tremors, at the first convulsive episode, and 240 minutes after the beginning of the urea feeding. Hyperammonemia already occured at the time of the first muscle tremors. Glucose and L-lactate levels were higher at the peak of the intoxication (convulsive episode), which were higher compared to the beginning of the experiment.Endogenous production of urea increased during the experiment due to hyperammonemia (r = 0.57), reaching peak levels at the end of the trials. Higher ammonia values lead to increased concentrations ofL-lactate, glucose, urea, creatinine and hematocrit values. These results showed that high levels of ammonia increased glyconeogenesis, anaerobic glycolysis, the endogenous synthesis of urea and the level of dehydration. L-lactate and glucose were the best variables to monitor biochemical changes in cases of ammonia poisoning

The measurement of urine pH to predict the amount of buffer used in the treatment of acute rumen lactic acidosis in cattle

The purpose of the present study was to establish a practical, fast, precise and low-cost procedure to estimate the degree of metabolic acidosis in cattle with acute rumen lactic acidosis for further treatment. The rumen acidosis was induced experimentally in 40 crossbreed rumen-cannulated 1.5-year-old steers. The induction caused the development of the most characteristic clinical signs of acute rumen lactic acidosis, severe rumen acidosis and a moderate metabolic acidosis, which was evidenced by low blood pH, and blood bicarbonate concentration and base excess (BE). A highly positive correlation (r=0.80) between urinary pH and BE concentration, and between urinary pH and blood pH (r=0.75) was observed. The BE concentration estimated by urinary pH was similar to that determined by venous blood gas analysis (P>0.99). Furthermore, the results presented by the predictive formula were very significant. In conclusion, urinary pH is a good tool to predict the quantity of buffers needed to treat metabolic acidosis in cattle with acute rumen lactic acidosis.

O presente estudo teve como objetivo desenvolver um procedimento de baixo custo, preciso, rápido e prático para estimar o grau de acidose metabólica, para tratar bovinos com quadros de acidose láctica ruminal. A acidose ruminal foi induzida experimentalmente em 40 novilhos mestiços de 1,5 anos de idade, implantados com cânula ruminal. Essa indução causou o surgimento de sinais clínicos muito típicos da enfermidade aguda, com o aparecimento de pronunciada acidose ruminal e acidose metabólica de grau moderado, caracterizado por baixo pH sangüíneo e diminutos teores de bicarbonato e excesso de base (BE) no sangue. Verificou-se uma alta correlação positiva (r = 0,80) entre o pH urinário e o BE e entre o pH urinário e o pH sangüíneo (r = 0,75). A concentração de BE estimado pelo pH urinário foi similar à obtida pela análise do hemogasômetro (P = 0,99). Além disso, os resultados apresentados pela fórmula de predição foram muito significativos. Dessa forma, conclui-se que a mensuração do pH urinário é uma boa alternativa para estimar a quantidade necessária de tampão para tratar o quadro de acidose metabólica em bovinos com acidose láctica ruminal aguda.

Avaliação do potencial da polpa cítrica em provocar acidose láctica ruminal aguda em bovinos / Comparative study of the citrus pulp to cause acute rumen lactic acidosis in cattle

Com o objetivo de avaliar o potencial da polpa cítrica (PC) em provocar acidose láctica ruminal aguda (ALRA), 15 bovinos com peso médio de 160 kg providos de cânula ruminal não-adaptados à dieta contendo concentrado foram alocados aleatoriamente em três grupos: CONTROLE - animais receberam apenas a dieta basal; SACAROSE - animais receberam sacarose diretamente no rumem a fim de provocar ALRA; POLPA - grupo que recebeu subitamente alta quantidade de PC no rúmen (equivalente a 1,65 % do peso corporal). Em vários tempos no decorrer de 24 horas, após administração dos substratos, foram determinados o volume globular, pH, excesso de bases (BE) e lactato total no sangue e pH e concentração de ácido láctico total no conteúdo ruminal. Exame clínico foi realizado no decorrer do 1º dia e o consumo de alimento acompanhado nos próximos sete dias. A administração de sacarose provocou um característico quadro de ALRA com o desenvolvimento de acidose ruminal e sistêmica, apatia, desidratação, diarréia e taquicardia. Por outro lado, a polpa cítrica produziu discreta e temporária acidose ruminal, atingindo na 6ª hora o pH ruminal mais baixo (5,35), sem provocar acidose sistêmica e quadro clínico mais evidente de ALRA, com exceção de uma diminuição temporária na ruminação e eliminação de fezes semilíquidas. A regularização do apetite ocorreu após dois dias no grupo com PC e sete dias no grupo com sacarose. Tais resultados indicam que a polpa cítrica pode ser utilizada na alimentação de bovinos com baixo risco de provocar ALRA.

With the aim to evaluate the risk of citrus pulp to induce acute rumen lactic acidosis (ARLA), 15 rumen cannulated cattle didn’t adapted to concentrates were randomly allocated in 3 groups: G1- CONTROL - group fed only the basal diet; G2 - SUCROSE – animals with ARLA induced by rumen administration of sucrose; G3 – CITRUS PULP – animals received citrus pulp into rumen (1.65 % of BW). Blood and rumen samples were drawn throughout the next 24 h to determine pH, lactic acid concentration and the packet cell volume, blood base excess. Clinical signs were also recorded and food intake followed by the next 7 days. Sucrose caused a systemic and ruminal acidosis and characteristic ARLA signs such as, apathy, dehydration, diarrhea and tachycardia, while citrus pulp gave rise to mild and brief rumen acidosis, reaching the lowest pH (5.35) at the 6th h, without any changing in the blood pH and any typical clinical sign, but temporary reduction in the rumination and excretion of semi liquid feces. Appetite was fully recovered after two and seven days in the pulp and sucrose group, respectively. These results showed that citrus pulp may be used as a feedstuff for cattle with low risk to cause ARLA.

Diagnóstico de carência energética em bovinos por testes de metabolismo ruminal / Diagnosis of energy deficiency in cattle by ruminal metabolism tests

Avaliou-se o metabolismo ruminal de bovinos submetidos ou não a dietas carentes em energia, por meio de provas bioquimicas e funcionais no fluido ruminal e urinário com finalidade diagnóstica. Para tal, foram utilizados 10 garrotes mestiços providos de cânula ruminal que foram divididos em dois grupos, ou seja: controle (C; n=4) dieta balanceada para ganho diário de 900 g e carência pronunciada de energia (CP; n=6) recebendo 30% a menos do nível de mantença em energia. Após os bovinos serem alimentados por 140 d foram coletadas amostras de fluido ruminal e urina antes da alimentação e nas 1ª, 3ª, 6ª e 9ª h seguintes. A carência energética provocou diminuição significativa nos teores ruminais de AGVs totais, ácidos propiônico e butírico, amônio, elevando-se o tempo da prova de redução do azul de metileno (RAM) e menor produção de gases no teste de fermentação de glicose (FG); o índice de excreção urinária de alantoína (IEVA) também foi menor. A carência provocou aumento na porcentagem molar de ácido acético. Não se verificou efeito dos tratamentos sobre o pH ruminal. Existiram correlações positivas de grande íntensidade entre FG e AGV s e amônia, e de média intensidade entre FG e amônia e lEVA, assim como de correlação negativa, de média íntensidade, entre RAM e AGV s, amônia, FG e lEVA. Com exceção do pH todas as análises estudadas detectaram alterações no metabolismo ruminal provocada pela carência energética. Porém, considerando-se a praticidade dos testes, recomenda-se a prova do RAM, seguida pela FG para um diagnóstico rápido e sensível deste quadro carencial.

Ten yearling crossbred rumen-cannulated steers were randomly divided in two equal groups for studying some ruminal metabolism tests in caule fed adequate or deficient diets on energy. The control group (C) was fed a diet to gain 900 g/BW / d, while to the very deficient group (VD) was given a diet with 30 % less than the maintenance level of dietary energy. On the 140th d ruminal fluid and urine samples were coliected at the basal and in the 1st, 3rd, 6th and 9th h after the morning feeding. The energy deficiency caused significant decrease in the ruminal levels of total volatile fatty acids (VFA), propionic and butyric acids, and ammonium, an increase in time of methilene blue reduction test (MBRT) and decrease in the gas production in the glucose fermentation test (GFT); the urinary aliantoin excretion rate (UAER) was also lower. The deficiency caused an increased in the molar proportion of acetic acid. There was no diet effect on the ruminal fluid pH. There were high positive correlation between GFT and VFAs and ammonium, medium positive correlation between MBRT and VFAs, ammonium, GFT and UAER. All studied variables were able to detect changes in the ruminal metabolism in caule fed energy deficient diet, but the rumen fluid pH. Nevertheless, as far as the feasibility is concerned the MBRT, foliowed by the GFT should be adopted to allow a rapid and sensible diagnosis of dietary energy deficiency.

Acute sheep poisoning from a copper sulfate footbath.

An outbreak of footrot occurred in a flock of Corriedale sheep; 27 animals were treated with antibiotic and footbathed in a 5% copper sulfate solution. Being deprived of water for > 17 h, many sheep drank the footbath solution. After 6 h 16 sheep became ill with acute copper poisoning, 10 animals died within 10 h; 6 were severely ill and were sent to Veterinary Hospital, and 4 had mild signs and recovered without treatment. The sick sheep had anorexia, dullness, grinding teeth, moaning, rumen atony, dehydration, dark blue-green diarrheic feces and congested membranes. They were treated with 3.4 mg tetrathiomolybdate/kg body weight and lactated Ringer's solution iv, oral molybdate, sulfate, kaolin and pectin, and drenched with antacids. Two of the 6 sheep died during hospitalization. The ingestion of copper solution caused an intense gastrointestinal injury that resulted in ulcers, petechial and echymotic hemorrhages in the mucosa, mild hemolysis detected by microscopic hemoglobinuria and a lowered packed cell volume, severe hepatic injury that raised the AST and gammaGT blood values, and moderate kidney lesions with increasing serum blood urea and nitrogen creatinine levels.

Experimental ammonia poisoning in cattle fed extruded or prilled urea: clinical findings

Doze garrotes Girolando, nunca alimentados com uréia, foram distribuídos em dois grupos de seis animais cada. Ambos os grupos receberam intraruminalmente dose única (0,5 g/kg PV) de uréia extrusada (G1) ou granulada (G2), para induzir quadro de intoxicação por amônia. O quadro clínico exibido pelos garrotes foi acompanhado durante 240 minutos. Além da constatação dos sinais clínicos clássicos ligados a essa intoxicação, o presente trabalho descreve a presença de três novos sinais: desidratação, hipotermia e vasos episclerais ingurgitados. Convulsão, considerada sinal definitivo, ocorreu em cinco de seis animais de cada grupo. Um garrote (G1) exibiu apenas fasciculações, enquanto outro (G2) desenvolveu quadro clínico típico, porém sem convulsão, e recuperou-se espontaneamente sem tratamento. Os surgimentos de tremores musculares, decúbito esternal e episódios convulsivos ocorreram em momentos similares em ambos os grupos, mas quando analisados conjuntamente verificou-se que foram mais tardios no G1 (p < 0,04). O 1º sinal clínico observado foi a fasciculação, seguida por apatia, hiperestesia, apoio em obstáculos, tremores musculares, atonia ruminal, incoordenação motora, decúbito esternal e lateral, desidratação leve ou severa, e convulsão. Maiores freqüências cardíacas foram detectadas na convulsão. Após a convulsão, quatro garrotes de cada grupo apresentaram hipotermia leve. Um garrote do G2 entrou em estado comatoso e sucumbiu subitamente antes que fosse iniciado o tratamento. Apesar da uréia extrusada adiar o surgimento do quadro clínico, os sinais evidenciados foram tão severos quanto os causados por uréia granulada. Ambas formas de uréia, oferecidas em altas doses são perigosas a bovinos que nunca foram alimentados com uréia.

A model for ammonia poisoning in cattle.

The intravenous infusion of ammonium chloride was used to induce ammonia (NH3) poisoning in cattle. A 1.5 M ammonium chloride solution, buffered to pH 7.0, was infused at 400 mL/h until a convulsive episode occurred and therapy was initiated. Convulsions occurred with 200 to 1200 mL of ammonium solution. The clinical picture and metabolic effects were similar to the natural poisoning; no side effected occurred. The hypermmoniemia caused hyperglycemia, hyperlactemia, hyperkalemia and Intense metabolic acidosis. After treatment there was a sharp decrease in plasma NH3. Within 110 min all steers stood and recovered appetites. The induction of NH3 poisoning in cattle with ammonium chloride offers many advantages over the administration of high po doses of urea.

Treatment of ammonia intoxication in rats with urea cycle amino acids, furosemide and fluids.

Three hundred sixty-seven male Wistar rats were used to compare the efficiency of urea cycle amino acids (arginine, citrulline and ornithine; Group O), furosemide (Group F), and fluid therapy (saline solution; Group FT) to treat ammonia toxicity. Rats were injected ip initially with an ammonium acetate solution at 99.9% of the lethal dose. Three min later the rats were allocated randomly to Group C (control, received 1.2 mL distilled water). Group O (amino acids listed earlier, 2 mmol/kg bw), Group F (furosemide, 2 mg/kg bw), Group FT (7mL saline), or Groups O+F, O+FT, F+FT, or O+F+FT. All treatments were given ip except for Group F given im injections. Plasma ammonia, urea and creatinine, and hematocrit and pulmonary dry matter were determined. The highest survival rates were obtained with O+FT (57%) and O+F+FT (62.5%); only 6% of the controls survived. Plasma ammonia levels were ten-fold lower in rats treated with O+FT and O+F+FT (p<0.0001). Fatally-poisoned rats had higher plasma ammonia, creatinine and hematocrit and exhibited pulmonary edema. Surviving rats had lower plasma urea. Animals given treatments with O, FT and F had (p<0.005) higher urea, lower creatinine and less severe pulmonary edema, respectively, than those untreated.