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Effect of exercise training and carvedilol treatment on cardiac function and structure in mice with sympathetic hyperactivity-induced heart failure 56
Medeiro,A.; Vanzelli,A.S.; Rosa,K.T.; Irigoyen,M.C.; Brum,P.C..
The present investigation was undertaken to study the effect of β-blockers and exercise training on cardiac structure and function, respectively, as well as overall functional capacity in a genetic model of sympathetic hyperactivity-induced heart failure in mice (α2A/α2CArKO). α2A/α2CArKO and their wild-type controls were studied for 2 months, from 3 to 5 months of age. Mice were randomly assigned to control (N = 45), carvedilol-treated (N = 29) or exercise-trained (N = 33) groups. Eight weeks of carvedilol treatment (38 mg/kg per day by gavage) or exercise training (swimming sessions of 60 min, 5 days/week) were performed. Exercise capacity was estimated using a graded treadmill protocol and HR was measured by tail cuff. Fractional shortening was...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Heart failure; Exercise training; Carvedilol treatment; Ventricular function; Cardiac remodeling; Α2A/α2CArKO mice.
Ano: 2008 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2008000900012
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Aerobic exercise training in heart failure: impact on sympathetic hyperactivity and cardiac and skeletal muscle function 56
Brum,P.C.; Bacurau,A.V.N.; Medeiros,A.; Ferreira,J.C.B.; Vanzelli,A.S.; Negrão,C.E..
Heart failure is a common endpoint for many forms of cardiovascular disease and a significant cause of morbidity and mortality. Chronic neurohumoral excitation (i.e., sympathetic hyperactivity) has been considered to be a hallmark of heart failure and is associated with a poor prognosis, cardiac dysfunction and remodeling, and skeletal myopathy. Aerobic exercise training is efficient in counteracting sympathetic hyperactivity and its toxic effects on cardiac and skeletal muscles. In this review, we describe the effects of aerobic exercise training on sympathetic hyperactivity, skeletal myopathy, as well as cardiac function and remodeling in human and animal heart failure. We also discuss the mechanisms underlying the effects of aerobic exercise training.
Tipo: Info:eu-repo/semantics/article Palavras-chave: Heart failure; Exercise training; Sympathetic hyperactivity; Ventricular function; Cardiac remodeling; Skeletal myopathy.
Ano: 2011 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2011000900002
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Overexpression of myeloid differentiation protein 88 in mice induces mild cardiac dysfunction, but no deficit in heart morphology 56
Chen,W.; Huang,Z.; Jiang,X.; Li,C.; Gao,X..
Cardiac remodeling involves changes in heart shape, size, structure, and function after injury to the myocardium. The proinflammatory adaptor protein myeloid differentiation protein 88 (MyD88) contributes to cardiac remodeling. To investigate whether excessive MyD88 levels initiate spontaneous cardiac remodeling at the whole-organism level, we generated a transgenic MyD88 mouse model with a cardiac-specific promoter. MyD88 mice (male, 20-30 g, n=∼80) were born at the expected Mendelian ratio and demonstrated similar morphology of the heart and cardiomyocytes with that of wild-type controls. Although heart weight was unaffected, cardiac contractility of MyD88 hearts was mildly reduced, as shown by echocardiographic examination, compared with wild-type...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Cardiac dysfunction; Cardiac remodeling; Transgenic mice; Myeloid differentiation protein 88.
Ano: 2016 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2016000100605
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YAP activation promotes the transdifferentiation of cardiac fibroblasts to myofibroblasts in matrix remodeling of dilated cardiomyopathy 56
Jin,Bo; Zhu,Jun; Shi,Hai-Ming; Wen,Zhi-Chao; Wu,Bang-Wei.
Yes-associated protein (YAP) is an important regulator of cellular proliferation and transdifferentiation. However, little is known about the mechanisms underlying myofibroblast transdifferentiation in dilated cardiomyopathy (DCM). We investigated the role of YAP in the pathological process of cardiac matrix remodeling. A classic model of DCM was established in BALB/c mice by immunization with porcine cardiac myosin. Cardiac fibroblasts were isolated from neonatal Sprague-Dawley rats by density gradient centrifugation. The expression levels of α-smooth muscle actin (α-SMA) and collagen volume fraction (CVF) were significantly increased in DCM mice. Angiotensin II (Ang II)-mediated YAP activation promoted the proliferation and transdifferentiation of...
Tipo: Info:eu-repo/semantics/article Palavras-chave: YAP; Fibroblast; Cardiac remodeling; Dilated cardiomyopathy.
Ano: 2019 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2019000100605
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Chronic aerobic exercise associated to low-dose L-NAME improves contractility without changing calcium handling in rat cardiomyocytes 56
Luchi,T.C.; Coelho,P.M.; Cordeiro,J.P.; Assis,A.L.E.M.; Nogueira,B.V.; Marques,V.B.; dos Santos,L.; Lima-Leopoldo,A.P.; Lunz,W.; Leopoldo,A.S..
Nitric oxide (NO) inhibition by high-dose NG-nitro-L-arginine methyl ester (L-NAME) is associated with several detrimental effects on the cardiovascular system. However, low-dose L-NAME increases NO synthesis, which in turn induces physiological cardiovascular benefits, probably by activating a protective negative feedback mechanism. Aerobic exercise, likewise, improves several cardiovascular functions in healthy hearts, but its effects are not known when chronically associated with low-dose L-NAME. Thus, we tested whether the association between low-dose L-NAME administration and chronic aerobic exercise promotes beneficial effects to the cardiovascular system, evaluating the cardiac remodeling process. Male Wistar rats were randomly assigned to control...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Nitric oxide; Aerobic exercise; Cardiac remodeling; Cardiomyocyte; Calcium.
Ano: 2020 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2020000300611
Registros recuperados: 5
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