Correlação entre os achados radiográficos e ecocardiográficos sugestivos de aumento cardíaco em cães: 104 casos / Correlation between radiographic and ecocardiographic findings suggestive of cardiomegaly in 104 dogs

Radiografias torácicas e ecocardiogramas de 104 caninos foram avaliados e correlacionados quanto ao aumento das câmaras cardíacas. Os achados radiográficos foram correlacionados estatisticamente a fim de se estabelecer a acurácia do exame radiográfico na detecção do aumento cardíaco em comparação ao ecocardiográfico - padrão-ouro não invasivo. A correlação entre os achados radiográficos indicativos de aumento cardíaco e os índices ecocardiográficos mostrou-se fraca, significativa somente para VHS versus relação átrio esquerdo/aorta (r=0,3136), eixo curto versus relação átrio esquerdo/aorta (r=0,3813) e eixo curto versus velocidade da onda E (r=0,2021). A acurácia da radiografia na determinação subjetiva de aumento das câmaras cardíacas foi razoável, variando entre 72,1% e 80,8%. Em contrapartida, o VHS apresentou baixa acurácia (50,9%) na detecção de cardiomegalia.(AU)

Thoracic radiographs and echocardiograms of 104 canines were evaluated and correlated regarding cardiac chambers enlargement. The radiographic findings were statistically correlated in order to establish the accuracy of the radiographic examination in the detection of cardiac enlargement in comparison with the echocardiogram - non-invasive gold standard. The correlation between the radiographic findings indicative of cardiac enlargement and echocardiographic indexes was weak, significant only for VHS versus left atrium to aorta ratio (r= 0.3136), short axis versus left atrium to aorta ratio (r= 0, 3813) and short axis versus E wave velocity (r= 0.2021). The radiographic accuracy in the subjective determination of cardiac chamber enlargement was reasonable, ranging from 72.1% to 80.8%. On the other hand, VHS presented low accuracy (50.9%) in the detection of cardiomegaly.(AU)

Estenose esofágica em duas cadelas após ovário-histerectomia: relato de caso / Esophageal stricture in two female dogs after ovariohysterectomy: case report

A estenose esofágica benigna é uma afecção rara em pequenos animais, comumente secundária a esofagites ulcerativas. O refluxo gastroesofágico, frequente durante procedimentos anestésicos, é a principal causa de esofagite grave, com consequente formação de cicatriz esofágica. O presente trabalho tem por objetivo descrever dois casos de estenose esofágica ocorrentes após ovário-histerectomia, com destaque para os procedimentos diagnósticos realizados. Em ambos os casos, a combinação dos sinais clínicos sugestivos e os achados de esofagograma e esofagoscopia foram determinantes. No primeiro caso, devido ao tempo avançado de desenvolvimento dos sinais clínicos, o paciente veio a óbito antes mesmo que a intervenção direta da região de estenose fosse realizada. Já no segundo, o procedimento de gastrostomia para melhor manejo alimentar, associado à dilatação esofágica via esofagoscopia e à terapia com medicamentos antiácidos, resultou em melhora clínica.(AU)

Benign esophageal stricture is a rare affection in small animals, usually secondary to ulcerative esophagitis. Gastroesophageal reflux, frequent during anesthetic procedures, is the main cause of severe esophagitis with consequent formation of esophageal cicatrix. The objective of this work is to describe two cases of esophageal stricture occurring after ovariohysterectomy, highlighting the diagnostic procedures performed. In both cases, the combination of the suggestive clinical signs and findings from an esophagram and an esophagoscopy were determinants. In the first case, due to the advanced stage of the clinical signs, the patient died before direct interventions on the stenosis region were performed. But in the second case, the gastrostomy procedures for better feed management associated with esophageal dilatation by esophagoscopy and therapy with antacids resulted in clinical improvement.(AU)

Avaliação dos valores de troponina I, eletrocardiograma e ecocardiograma em felinos sedados com cetamina e midazolam, suplementados ou não com oxigênio / Troponin I, electrocardiography and echocardiography values in felines sedated with ketamine and midazolam, supplemented or not with oxygen

Lesões no miocárdio, causadas por baixa perfusão e oxigenação cardíaca, podem ser ocasionadas por fármacos anestésicos, como a cetamina. Essas lesões podem ser identificadas por meio de biomarcadores específicos e, dentre estes, destaca-se a troponina I. O objetivo deste estudo foi avaliar as alterações cardiovasculares com base nos valores de troponina I (TnI), eletrocardiograma (ECG) e ecocardiograma em gatos sedados com cetamina e midazolam, suplementados ou não com oxigênio. Utilizaram-se 12 gatos machos, hígidos, nos quais se avaliaram os valores de troponina I, eletro e ecocardiografia, frequência cardíaca (FC) e pressão arterial sistólica (PAS) no momento basal (M0). Na sequência, os animais foram sedados com a associação de 10mg.kg-1 de cetamina e 0,5mg.kg-1 de midazolam pela via intramuscular. Decorridos aproximadamente 10 minutos, os animais foram alocados aleatoriamente em dois grupos: com e sem suplementação de oxigênio via máscara facial (GCO e GSO, respectivamente), sendo submetidos novamente aos exames citados. Foram coletadas amostras sanguíneas, para dosagem de TnI em seis, 12 e 24 horas após a administração dos agentes anestésicos. Não foram observadas alterações significativas na FC, na PAS e no ECG após a administração dos tratamentos em ambos os grupos. Os valores médios de TnI elevaram-se significativamente em T6 quando comparados ao basal em ambos os grupos, com médias de 0,507±0,335ng/mL no GSO e 0,777±0,505ng/mL no GCO. Na ecocardiografia, o débito cardíaco (DC) reduziu em M1 em ambos os grupos, quando comparados aos valores basais, sendo M0 0,472±0,115 e M1 0,234±0,08 no GSO e M0 0,356±0,095 e M1 0,222±0,09 no GCO, expressos em L/min. Conclui-se que a administração de cetamina e midazolam em gatos hígidos não promove alterações eletrocardiográficas, aumenta os valores de troponina I, com pico de seis horas após a administração, reduz o débito cardíaco, e que a suplementação de oxigênio 100% via máscara facial não atenua tais alterações.

Myocardium injuries caused by low myocardial oxygenation and perfusion might be induced by anesthetics agents like ketamine. These injuries can be detected by specific biomarkers and, among them, troponin I. The aim of this study was to evaluate the cardiovascular changes based on troponin I (TnI) values, electrocardiography (ECG) and echocardiography in cats sedated with ketamine and midazolam, supplemented or not with oxygen. Blood samples were collected from 12 intact male healthy cats for troponin I (T0) and they were then submitted to electrocardiographic and echocardiographic evaluation, as well as measurements of heart rate (HR) and systolic blood pressure (SBP) (M0). Subsequently, they were ketamine-midazolam (10mg.kg-1 and 0,5 mg.kg-1 respectively) anesthetized by intramuscular route. After about 10 minutes, the animals were randomly allocated into two groups with or without oxygen supplementation (GCO or GSO, respectively), again being subjected to the tests mentioned. Blood samples for troponin I were collected at 6, 12 and 24 hours after sedation. HR, SBP and ECG did not change among groups. The TnI values rise significantly in T6 comparing to baselines in both groups (0,507±0,335 ng/mL in GSO and 0,777±0,505 ng/mL in GCO). In echocardiography, the cardiac output decreased at M1, in both groups compared to baseline (M0 0,472±0,115 and M1 0,234±0,08 in GSO and M0 0,356±0,095 and 0,222±0,09 in GCO, L/min). We concluded that ketamine and midazolam sedation in healthy cats did not cause changes electrocardiography, increase troponin I values, with an 6 hours peak after administration, reduces cardiac output and oxygen supplementation, via facial mask, did not attenuated these alterations.

Hypothalamic regulatory peptides in obese and lean Zucker rats.

1. Hypothalamic concentrations of nine peptides with experimental effects on energy balance were compared in obese (fa/fa) and lean (Fa/?) male Zucker rats. To determine whether any peptide differences between obese and lean rats might be due to the overweight condition per se, separate groups of obese rats were food-restricted to reduce their body weight to lean values. 2. Concentrations of neuromedin B, a bombesin-like peptide, in the central hypothalamus were significantly higher in obese than in lean rats. This difference was not affected in food-restricted obese rats. 3. Hypothalamic levels of neuropeptide Y, an extremely potent central appetite stimulant, were similar in lean and freely fed obese rats but central hypothalamic levels of neuropeptide Y rose significantly in food-restricted obese rats. 4. These findings suggest that disturbances in hypothalamic neuromedin B concentrations may be involved in the obesity syndrome of the fa/fa Zucker rat. Increased central hypothalamic levels of neuropeptide Y in food-restricted rats suggest that this peptide may help to defend body weight by stimulating eating after weight loss.

Hypothalamic regulatory peptide disturbances in the spontaneously obese JCR: LA-corpulent rat.

Central and lateral hypothalamic concentrations of 9 regulatory peptides implicated in the control of feeding behaviour were measured in corpulent (cp/cp) JCR:LA-cp rats which develop spontaneous obesity, hyperinsulinaemia and hyperlipidaemia, and in lean (+/?) controls. In female cp/cp rats, central hypothalamic levels of neuropeptide Y (NPY), neurotensin, somatostatin and substance P were significantly lower (p less than 0.02) than in lean female controls. Following food restriction with a 16% reduction in body weight, these differences were apparently reversed and there were also significant rises in the lateral hypothalamic concentrations of neurotensin and of galanin. The other 4 peptides examined (bombesin, calcitonin gene-related peptide, neuromedin B and vasoactive intestinal peptide) did not differ significantly between cp/cp and lean females, either fed freely or food-restricted. Male cp/cp rats showed no significant differences from lean males in central or lateral hypothalamic concentrations of any of the 9 peptides. NPY and galanin are powerful and specific central appetite stimulants, whereas neurotensin, substance P and somatostatin inhibit feeding when injected centrally. Disturbances in these putative appetite-regulating peptides may be involved in the hyperphagia and other hypothalamic abnormalities in this spontaneous obesity syndrome. The apparent absence of differences between the male corpulent and lean groups may relate to sexual dimorphism of the syndrome, which is more marked in the females.

Elevated neuropeptide Y concentrations in the central hypothalamus of the spontaneously diabetic BB/E Wistar rat.

Insulin-deficient diabetes causes hypothalamic and pituitary dysfunction. The possible role of hypothalamic regulatory peptides in mediating these disturbances was investigated in spontaneously diabetic BB/E Wistar rats. Concentrations of 10 regulatory peptides were measured in the central (nucleus-rich) and lateral parts of the hypothalamus in 18 diabetic and 5 non-diabetic BB/E rats. Diabetic rats were treated with either intensified or low-dose insulin schedules to achieve moderate or severe hyperglycaemia (mean blood glucose concentrations, 8 and 20 mmol l-1 respectively). Neuropeptide Y concentration and content in the central hypothalamus were increased by 30-40% in both moderately and severely hyperglycaemic diabetic groups (p less than 0.01). Lateral hypothalamic neuropeptide Y levels did not differ significantly between the groups. The only other peptide to show any significant difference between diabetic and control rats was calcitonin gene-related peptide, whose central hypothalamic concentrations were significantly increased in the severely hyperglycaemic animals. Alterations of hypothalamic neuropeptide Y, which has potent experimental effects on hypothalamo-pituitary function, may contribute to certain neuroendocrine disturbances in insulin-deficient diabetes.

Increased neuropeptide Y concentrations in specific hypothalamic regions of streptozocin-induced diabetic rats.

Untreated streptozocin-induced diabetic (STZ-D) rats have previously been shown to have significantly increased hypothalamic concentrations of neuropeptide Y (NPY), a regulatory peptide that powerfully stimulates eating and drinking and inhibits secretion of several pituitary hormones when injected centrally. Tissue NPY concentrations have been measured by radioimmunoassay in selected hypothalamic regions microdissected from fresh, unfixed brain slices to localize diabetes-associated NPY changes precisely within the hypothalamus. Significant (35-200%) increases in NPY concentrations (P less than .01 vs. matched nondiabetic controls) were found in specific hypothalamic regions between 3 and 14 wk after induction of STZ-D. These regions included the paraventricular and ventromedial nuclei and lateral hypothalamic area, major appetite-regulating areas that are sensitive to the hyperphagic and polydipsic actions of NPY. Increased NPYergic activity in these areas may, at least partly, drive the increased eating and drinking characteristic of STZ-D. NPY concentrations were also increased in the arcuate nucleus and medial preoptic area. Because both of these regions are important in modulating pituitary hormone secretion, local NPY increases may be involved in the impaired secretion of luteinizing hormone, thyroid-stimulating hormone, growth hormone, and prolactin known to occur in STZ-D. Our finding of NPY increases in specific hypothalamic nuclei associated with functional changes found in STZ-D suggests that this peptide may have a role in the altered metabolic and neuroendocrine regulation of the syndrome.