147 resultados para heart muscle injury


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The objective was to evaluate serum activity of the enzymes creatine kinase (CK) and aspartate aminotransferase (AST), which are leakage enzymes responsive to muscle injury, of athletic horses that underwent muscle biopsy and incremental jump test (IJT) involving incremental jumps. The animals were grouped as follows: the first group, horses with history of superior performance (SP); the second, with a history of inferior performance (IP); and lastly, a control group (CG). All groups underwent biopsy of the gluteus medius muscle, while groups SP and IP were also submitted to the incremental jump test (IJT) 24 hours after biopsy. The IJT consisted of three stages with 40 jumps each, where jump height increased progressively, from 40 to 60 and last, 80cm. Blood samples were drawn before biopsy, and 6 and 24 hours after the exercise as well. The levels of CK serum activity increased 6 hours after exercise and decreased 24 hours later in all groups, including CG. AST activity did not increase after biopsy and exercise. There was no increase of both enzyme activities that could be attributed to the exercise, possibly due to exercise short duration and/or low intensity. We conclude that the muscle biopsy was able to show that there was enough stimulus to cause CK enzyme leakage into the plasma, and consequent detection of increased serum activity, while the incremental jump test did not.

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Pós-graduação em Biologia Geral e Aplicada - IBB

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Este estudo visou verificar o efeito da sonoforese com Arnica montana sobre a fase inflamatória aguda de uma lesão muscular. Para isso, 40 ratos Wistar machos, lesados cirurgicamente, foram divididos em 4 grupos: controle (C), 10 ratos lesados e não tratados; grupo ultra-som (US), 10 lesados, tratados com US; grupo ultra-som com arnica (US+A), 10 ratos lesados, tratados com sonoforese de gel de arnica; grupo arnica (A), 10 ratos lesados, tratados com massagem de gel de arnica. O tratamento dos três grupos foi iniciado 24h após a lesão, sendo aplicado uma vez ao dia durante 3 minutos, por três dias. Quatro dias após a lesão, os animais foram sacrificados e o terço médio do músculo tibial anterior lesado foi removido e tratado histologicamente. Os resultados da análise qualitativa mostram que, no grupo C, formou-se um intenso infiltrado de células inflamatórias no espaço intersticial e um processo de regeneração apenas iniciado. Nos grupos US e US+A foi detectado um avançado processo inflamatório, com tecido conjuntivo mais organizado e consistente. No grupo A foi detectada diminuição no número de células inflamatórias e uma desorganização em sua disposição, o que poderia levar a um atraso no processo de regeneração. Conclui-se que os grupos que receberam a aplicação do ultra-som e ultra-som com arnica apresentaram semelhante aceleração do processo inflamatório agudo, sugerindo ineficácia da sonoforese quando comparada à aplicação de apenas ultra-som.

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A síndrome da cauda flácida é uma enfermidade que acomete cães de caça, principalmente Labradores Retriever e do grupo Pointer. Embora sua etiologia não esteja totalmente definida, sabe-se que sua ocorrência é precedida de esforço físico extenuante, exposição ao frio ou água fria e confinamento em caixas de transporte. O presente trabalho descreve o caso de um cão da raça Labrador Retriever, macho não castrado, de quatro anos de idade que apresentou súbita dor e flacidez da cauda após banho frio. Fratura vertebral, síndrome da cauda eqüina, outras enfermidades da medula espinhal ou de glândulas adanais e afecções prostáticas foram descartadas após exames auxiliares. A divulgação deste relato é relevante uma vez que esta síndrome ainda não foi descrita no Brasil.

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In order to test if the maximal velocity of shortening (V(max)TP) reflects the level of inotropism and is affected by preload and afterload, the behavior of this index was compared in two groups of anesthetized, atropinized dogs when preload and afterload were raised with an angiotensin II infusion. In seven dogs (group I), the arterial pressure elevation was allowed to inhibit reflectively the sympathetic tone and depress contractility. In eleven dogs (group II), the adrenergic activity was abolished by previous administration of reserpine. In group I, there was a significant decrease in V(max)TP during the angiotensin infusion. In group II, there was no significant change in the value of this index when the drug was infused. In six animals of this group, a further increase of arterial pressure was induced, but the values of V(max)TP remained similar to control. These results suggest that this index reflects the inotropic state of the myocardium and does not suffer significantly from the influence of preload and afterload elevations within our experimental limits.

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Inotropic effects of Propafenon were studied in isovolumic isolated guinea pig hearts submitted to infusion of the drug during 10 minutes. The dosages utilized caused: bradycardia, depression of AV nodal conduction and QRS widening. Simultaneously there was: decrease of the developed pressure (DP) and of the rate of rise of pressure (dp/dt), and elongation of the time of peak pressure. Since there was no clear relation between the heart rate and the inotropic indices (PD and dp/dt), it could be supposed that the depressor effect was not due to impairment of the chronotropism only. After the infusion of Propafenon, the chronotropic effect disapeared after 15 min, while the inotropic state presented a less satisfatory recuperation. The coronary output accompanied the myocardial metabolic needs, that is to say, there was a fall during the period of depressed cardiac function and a later tendency to increase during recovery.

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The relationship between coronary sinus blood oxygen tension (CSPO 2) and myocardial oxygen tension (MPO 2) variations during cardiac ischemia and reperfusion was studied in anesthetized open-chest dogs. Oxygen tension was measured by a polarographic method. Ischemia resulted in a slightly decreased CSPO 2 and a more pronounced reduction of MPO 2. After reperfusion the CSPO 2 rose rapidly and transiently before it returned gradually to the control level. By contrast, during the recovery period, the MPO 2 increased slowly, with recovery occurring long after the peak of CSPO 2. These data suggest that during the reperfusion phase, the CSPO 2 variation is probably due to opening of the myocardial arteriovenous shunts instead of an increase of flow through the myocardial capillary bed.

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The rate removal of nickel from the airway was measured in vivo. Removal in vivo was studied by intratracheal injection of nickel chloride solutions. Regardless of time after injection, the lungs and heart retained the greatest concentration of nickel and 40 days after 1.68 mumol administration they were the organs where nickel was still significantly measurable. The slow removal of nickel may indicate the presence of high affinity binding sites in the lung. Nickel can interact with others metals, such as copper and zinc, so that nickel exposure may have public health implications.