O Treinamento físico por natação atenua o remodelamento miocárdico e congestão pulmonar em ratas wistar com insuficiência cardíaca secundária a infarto do miocárdio

Portes, Leslie Andrews; Tucci, Paulo José Ferreira

doi:10.1590/s0066-782x2006001400008

Cited by 9 publications

(14 citation statements)

References 41 publications

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“…The muscle cross-sectional area (CSA) was calculated from the muscle weight and length by assuming cylindrical uniformity and a specific gravity of 1. The values were normalized to conform to previous publications [15]–[19]. After the papillary muscle was removed, left and right ventricles were separated and weighed for posterior evaluation of biometrical parameters.…”

Section: Methodsmentioning

confidence: 99%

Treadmill Exercise Training Prevents Myocardial Mechanical Dysfunction Induced by Androgenic-Anabolic Steroid Treatment in Rats

et al. 2014

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Elevated concentrations of testosterone and its synthetic analogs may induce changes in cardiovascular function. However, the effects of the combination of anabolic/androgenic steroid (AAS) treatment and exercise training on systolic and diastolic cardiac function are poorly understood. In the present study, we aimed to investigate the effects of low-dose steroid treatment (stanozolol) on cardiac contractile parameters when this steroid treatment was combined with exercise training in rats and the effects of chronic steroid treatment on the Frank-Starling (length-tension curves) relationship. Male Wistar rats were randomly assigned to one of four groups: U (untrained), US (untrained and treated with stanozolol 5 mg/kg/week), T (trained, 16 m/min/1 h) and TS (trained and treated with stanozolol 5 mg/kg/week). Continuous exercise training was conducted 5 days/week for 8 consecutive weeks. The speed of the treadmill was gradually increased to a final setting of 16 m/min/1 h. Experiments were divided into two independent series: 1) central hemodynamic analysis for mean arterial blood pressure (MAP) and cardiac output (CO) measurements and 2) isolated papillary muscle preparation in Krebs solution. Stanozolol treatment significantly increased the MAP and the heart size in untrained and trained rats (U 113±2; T 106±2; US 138±8 and TS 130±7 mmHg). Furthermore, stanozolol significantly decreased developed tension and dT/dt (maximal and minimal) in U rats. However, the developed tension was completely restored by training. The Frank/Starling relationship was impaired in rats treated with stanozolol; however, again, training completely restored diastolic function. Taken together, the present data suggest that AAS treatment is able to decrease cardiac performance (systolic and diastolic functions). The combination of stanozolol and physical training improved cardiac performance, including diastolic and systolic functions, independent of changes in central hemodynamic parameters. Therefore, changes in ventricular myocyte calcium transients may play a cardioprotective role.

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Section: Methodsmentioning

confidence: 99%

Treadmill Exercise Training Prevents Myocardial Mechanical Dysfunction Induced by Androgenic-Anabolic Steroid Treatment in Rats

et al. 2014

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“…The wet weight of the lung was measured and the tissue was then placed in an oven at 60°C for 24 h. The lungs water content (%H 2 O) was determined as follows [15]: %H 2 O = (wet weight - dry weight)/wet weight × 100. Cardiac wet weight was used to determine the cardiac weight/body weight ratio.…”

Section: Methodsmentioning

confidence: 99%

Cardiac and vascular changes in elderly atherosclerotic mice: the influence of gender

et al. 2010

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BackgroundAlthough advanced age is considered a risk factor for several diseases, the impact of gender on age-associated cardiovascular diseases, such as atherosclerotic processes and valvular diseases, remains not completely clarified. The present study was designed to assess aortic valve morphology and function and vascular damage in elderly using the apolipoprotein E knockout (ApoE KO) mouse. Our hypothesis was that advanced age-related cardiovascular changes are aggravated in atherosclerotic male mice.MethodsThe grade (0 to 4) of aortic regurgitation was evaluated through angiography. In addition, vascular lipid deposition and senescence were evaluated through histochemical analyses in aged male and female ApoE KO mice, and the results were compared to wild-type C57BL/6J (C57) mice.ResultsAortic regurgitation was observed in 92% of the male ApoE KO mice and 100% of the male C57 mice. Comparatively, in age-matched female ApoE KO and C57 mice, aortic regurgitation was observed in a proportion of 58% and 53%, respectively. Histological analysis of the aorta showed an outward (positive) remodeling in ApoE KO mice (female: 1.86 ± 0.15; male: 1.89 ± 0.68) using C57 groups as reference values. Histochemical evaluation of the aorta showed lipid deposition and vascular senescence only in the ApoE KO group, which were more pronounced in male mice.ConclusionThe data show that male gender contributes to the progression of aortic regurgitation and that hypercholesterolemia and male gender additively contribute to the occurrence of lipid deposition and vascular senescence in elderly mice.

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“…The electrocardiogram 2 and the echocardiogram [3][4][5][6][7][8][9][10][11][12][13][14][15] are noninvasive methods capable of identifying the area of necrosis or scarring. Although it identifies the presence of an MI-dependent electrically inactive area, the ECG is not a method that can quantify the infarction area 2 .…”

Section: Introductionmentioning

confidence: 99%

“…Although it identifies the presence of an MI-dependent electrically inactive area, the ECG is not a method that can quantify the infarction area 2 . The echocardiogram can determine the presence and the size of the MI with very good sensitivity [3][4][5][6][7][8][9][10][11][12][13][14][15] , even in periods as early as two days after necrosis, and it also provides information about deviant atrial and ventricular function. The best method for post-mortem diagnosis of MI depends on the stage in which the autopsy occurs.…”

Section: Introductionmentioning

confidence: 99%

Características fisiopatológicas do modelo de insuficiência cardíaca pós-infarto do miocárdio no rato

Tucci¹

2011

Arq. Bras. Cardiol.

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Congestive heart failure (CHF) caused by myocardial infarction in rats is the most commonly used experimental model to study the congestive heart failure syndrome. Following myocardial necrosis, the manifestations observed in rats very satisfactorily reproduce the findings in humans with cardiac decompensation and substantiate the study of CHF pathogenesis, pathophysiology, and treatment. Two features are inadequate in the model: the high mortality rate in the first 24 hours after coronary occlusion, and the considerable diversity of myocardial infarct sizes. In this review we described methodological and pathophysiological aspects of the model, concluding with a reference to an alternative technique, which uses radio frequency electric current to produce myocardial necrosis, and evolves with low mortality rates and homogeneous infarct sizes.For years, congestive heart failure (CHF) has been among the most investigated topics in cardiology. Besides the information obtained in humans, contribution made by the research conducted in laboratory animals is also noteworthy. Among the several experimental models available, the most used is that which promotes a congestive heart syndrome by the induction of myocardial necrosis in rats. Its current popularity and the foreseen increased interest in this model stress the importance of describing the pathophysiological characteristics after myocardial infarction (MI) in rats. Recently, a valuable literature review on the rat myocardial infarction model was published in the Arquivos Brasileiros de Cardiologia 1 .Although useful for the assessment of the congestive syndrome and the myocardial remodeling that occurs in the remaining cardiac muscle, the pathophysiological process established in rats after coronary artery ligation is not analogous to what happens in human coronary syndromes. The model lacks the arterial lesions that determine the distinctive clinical profile of human coronary artery disease: arrhythmias, transient ischemia, and recurrence of coronary occlusion, which are absent in laboratory animals.Occlusion of the anterior interventricular coronary artery is the strategy most frequently used for the induction of MI.The electrocardiogram 2 and the echocardiogram [3][4][5][6][7][8][9][10][11][12][13][14][15] are noninvasive methods capable of identifying the area of necrosis or scarring. Although it identifies the presence of an MI-dependent electrically inactive area, the ECG is not a method that can quantify the infarction area 2 . The echocardiogram can determine the presence and the size of the MI with very good sensitivity [3][4][5][6][7][8][9][10][11][12][13][14][15] , even in periods as early as two days after necrosis, and it also provides information about deviant atrial and ventricular function. The best method for post-mortem diagnosis of MI depends on the stage in which the autopsy occurs. In the first days after myocardial necrosis, the histopathologic exam may be inconclusive as to the limits of the necrotic area. For this phase, the triphe...

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O Treinamento físico por natação atenua o remodelamento miocárdico e congestão pulmonar em ratas wistar com insuficiência cardíaca secundária a infarto do miocárdio

Abstract: The increase of cardiac mass and pulmonary water content presented by MIlg-SED was diminished in the trained animals. The results suggest that the practice of physical exercise can diminish HF and contribute to favorable cardiac remodeling.

Cited by 9 publications

References 41 publications

Treadmill Exercise Training Prevents Myocardial Mechanical Dysfunction Induced by Androgenic-Anabolic Steroid Treatment in Rats

Treadmill Exercise Training Prevents Myocardial Mechanical Dysfunction Induced by Androgenic-Anabolic Steroid Treatment in Rats

Cardiac and vascular changes in elderly atherosclerotic mice: the influence of gender

Características fisiopatológicas do modelo de insuficiência cardíaca pós-infarto do miocárdio no rato

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