3 resultados para STRESS MYOCARDIAL PERFUSION SCINTIGRAPHY
em Repositório da Universidade Federal do Espírito Santo (UFES), Brazil
Resumo:
Myocardial infarction leads to compensatory ventricular remodeling. Disturbances in myocardial contractility depend on the active transport of Ca2+ and Na+, which are regulated by Na+-K+ ATPase. Inappropriate regulation of Na+-K+ ATPase activity leads to excessive loss of K+ and gain of Na+ by the cell. We determined the participation of Na+-K+ ATPase in ventricular performance early and late after myocardial infarction. Wistar rats (8-10 per group) underwent left coronary artery ligation (infarcted, Inf) or sham-operation (Sham). Ventricular performance was measured at 3 and 30 days after surgery using the Langendorff technique. Left ventricular systolic pressure was obtained under different ventricular diastolic pressures and increased extracellular Ca2+ concentrations (Ca2+e) and after low and high ouabain concentrations. The baseline coronary perfusion pressure increased 3 days after myocardial infarction and normalized by 30 days (Sham 3 = 88 ± 6; Inf 3 = 130 ± 9; Inf 30 = 92 ± 7 mmHg; P < 0.05). The inotropic response to Ca2+e and ouabain was reduced at 3 and 30 days after myocardial infarction (Ca2+ = 1.25 mM; Sham 3 = 70 ± 3; Inf 3 = 45 ± 2; Inf 30 = 29 ± 3 mmHg; P < 0.05), while the Frank-Starling mechanism was preserved. At 3 and 30 days after myocardial infarction, ventricular Na+-K+ ATPase activity and contractility were reduced. This Na+-K+ ATPase hypoactivity may modify the Na+, K+ and Ca2+ transport across the sarcolemma resulting in ventricular dysfunction.
Resumo:
O objetivo desse trabalho foi obter estimativas da tensão de crescimento longitudinal em árvores vivas e verificar a sua relação com algumas características da madeira de Eucalyptus dunnii Maiden aos oito, treze, quinze e dezenove anos de idade. O material foi proveniente da Empresa Procopiak Compensados e Embalagens S.A., localizada no Município de Canoinhas, Santa Catarina. Os níveis de tensão longitudinal de crescimento foram mensurados indiretamente pelo método do "CIRAD-Forêt", na árvore viva, e estimados a partir do módulo de elasticidade dinâmico e do módulo de elasticidade obtido no ensaio de tração paralela à grã. A deformação residual longitudinal (DRL) e as estimativas das tensões de crescimento longitudinais apresentaram tendência de aumento, na média, com a idade do material. A DRL apresentou correlação, positiva e significativa, com todas as estimativas das tensões de crescimento longitudinais, sendo de maior magnitude aos 13, 15 e 19 anos de idade. A densidade básica apresentou maiores correlações, positivas e significativas, com o módulo de elasticidade dinâmico, estimado no sentido longitudinal, para a madeira na condição de saturação e a 12% de umidade, em todas as idades avaliadas. Todas as estimativas das tensões de crescimento longitudinais apresentam elevadas correlações, positivas e significativas, entre si.
Resumo:
Myocardial contractility depends on several mechanisms such as coronary perfusion pressure (CPP) and flow as well as on a1-adrenoceptor stimulation. Both effects occur during the sympathetic stimulation mediated by norepinephrine. Norepinephrine increases force development in the heart and produces vasoconstriction increasing arterial pressure and, in turn, CPP. The contribution of each of these factors to the increase in myocardial performance needs to be clarified. Thus, in the present study we used two protocols: in the first we measured mean arterial pressure, left ventricular pressure and rate of rise of left ventricular pressure development in anesthetized rats (N = 10) submitted to phenylephrine (PE) stimulation before and after propranolol plus atropine treatment. These observations showed that in vivo a1-adrenergic stimulation increases left ventricular-developed pressure (P<0.05) together with arterial blood pressure (P<0.05). In the second protocol, we measured left ventricular isovolumic systolic pressure (ISP) and CPP in Langendorff constant flow-perfused hearts. The hearts (N = 7) were perfused with increasing flow rates under control conditions and PE or PE + nitroprusside (NP). Both CPP and ISP increased (P<0.01) as a function of flow. CPP changes were not affected by drug treatment but ISP increased (P<0.01). The largest ISP increase was obtained with PE + NP treatment (P<0.01). The results suggest that both mechanisms, i.e., direct stimulation of myocardial a1-adrenoceptors and increased flow, increased cardiac performance acting simultaneously and synergistically.