Caracterização funcional da hipertrofia miocárdica induzida pelo isoproterenol e de sua regressão

Murad, Neif; Franco, Marcello; Tucci, Paulo José Ferreira

doi:10.1590/s0066-782x2001000700005

Cited by 3 publications

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“…In a study of hearts isolated from rats with hypertrophy induced by repeated subcutaneous administration of ISO, we noted that the variation in left ventricle (LV) volume necessary to increase diastolic pressure from 0 to 40 mmHg (ΔV 40 ) differed markedly among hypertrophied hearts. 21 In some hearts, ΔV 40 was similar to values observed in normal hearts, whereas in others it was clearly lower than normal. The aim of the present study was to analyse whether this difference in ventricular distensibility bears evidence that ISO‐induced hypertrophy can lead to distinct cardiac structural and functional patterns.…”

Section: Introductionsupporting

confidence: 51%

Isoproterenol‐Induced Hypertrophy May Result In Distinct Left Ventricular Changes

Murad

Tucci

2000

Clin Exp Pharma Physio

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1. The aim of the present study was to analyse the possible lack of uniformity in isoproterenol (ISO)-induced myocardial hypertrophy. 2. Data obtained for isovolumic hearts isolated from 20 rats treated with ISO (0.3 mg/kg over 8 days) were divided into two groups (H1, n = 10; H2, n = 10) according to the volume (mean+/-SD) needed to change left ventricle diastolic pressure from 0 to 40 mmHg (H1, 184+/-30 microL; H2, 108+/-14 microL). Eight control rats (C; 165+/-37 microL) were used for comparison. 3. In addition to ventricular distensibility differences, the groups differed in terms of myocardial mass (mean+/-SEM: H1, 181+/-3 mg > H2, 166+/-3 mg > C, 136+/-3 mg; P < 0.001), of relaxation constant (H2, 43+/-4 msec > H1, 28+/-2 msec; P = 0.0012) and of maximum developed circumferential stress (C, 145+/-9 kdyn/cm2 = H1, 137+/-6 kdyn/cm2 > H2, 110+/-4 kdyn/cm2; P = 0.002). 4. Our results show that ISO-induced myocardial hypertrophy is not homogeneous. Data obtained for H2, taken as a whole and compared with H1 (smaller myocardial mass and impairment of relaxation, elastic stiffness and force generation), suggest that, in some animals, myocardial necrosis and reparative fibrosis may prevail over the stimulus for myocyte growth. The lack of uniformity of ISO-induced myocardial hypertrophy has not been previously reported and may have contributed to the divergence observed in the literature regarding the functional characteristics of the present model.

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Section: Introductionsupporting

confidence: 51%

Isoproterenol‐Induced Hypertrophy May Result In Distinct Left Ventricular Changes

Murad

Tucci

2000

Clin Exp Pharma Physio

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“…CMH possui característica mendeliana com um padrão de herança autossômica dominante, que em grande parte é causada por uma variedade de mutações em genes que codificam proteínas do sarcômero (Figura 3) (β-miosina de cadeia pesada, Troponina cardíaca T, α-Tropomiosina, Proteína C de ligação à miosina e na cadeia leve de miosina ocorre mais raramente) (Maron, 2002;Spirito et al, 1997), caracterizada pelo envolvimento do ventrículo esquerdo (VE) simétrico (concêntrica) ou assimétrico (septal, medioventricular, apical, lateral e posterior) (Albanesi, 1996), hipertrofiado não dilatado com desarranjo miofibrilar e evidente fibrose intersticial e perivascular (Figura 4) no miocárdio (Maron, 1997;Murad et al, 2001;Hu et al, 2003;Ommen e Nishimura, 2004;Poliac et al, 2006; Harvey e Leinwand, 2011), tendo aumento das dimensões dos cardiomiócitos (Franchini, 2001) e muitas vezes ocorrendo em especial no septo interventricular (Seidman e Seidman, 2001 Figura 5 -(A) Espécime patológico de um paciente que morreu subitamente com CMH (Ommen et al, 2011). (B) Coração normal, com espessura e dimensões normais do VE Do ponto de vista hemodinâmico, as CMH são divididas em obstrutivas (septal assimétrica e medioventricular) e não obstrutivas (septal assimétrica, concêntrica, apical, lateral e/ou látero-posterior) (Albanesi, 1996).…”

Section: Cardiomiopatia Hipertróficaunclassified

Efeitos cardiopulmonares da exposição ao material particulado fino (MP2,5) proveniente do concentrador de partículas ambientais (CPA) na hipertrofia ventricular esquerda de ratos wistar

Belotti¹

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Aos amigos Luiz Afonso Pires, Mac Gayver da Silva Castro e RobsonSeriani pela amizade e companheirismo durante o todo o período de estudo e divertimento.Ao Guilherme, Gabriel e Laís minha sincera gratidão pela ajuda e dedicação que foram oferecidas neste trabalho. Epidemiological and experimental studies have consistently shown that both short-and long-term exposures to air pollution are associated with a variety of cardiovascular diseases. Air pollution is composed by a mixture of noxious substance including particles and gases. The cardiovascular adverse effects are more commonly attributed to particles and toxicological experiments have demonstrated several mechanisms by which particle exposure may trigger these effects. In this study we investigated the effects of time (7, 15 and 21 days) of exposure to concentrated ambient particles (dose = 600 µg/m³) on morphofunctional parameters of the heart in normal and rats with left ventricular hypertrophy (LVH) induced by isoproterenol (nonselective β-adrenergic agonist with direct action) (1.2 mg/kg). The use of LVH rats was motivated by the fact that individuals with cardiovascular diseases are considered at higher risk for effect of ambient PM. Our data have shown that time is an important factor on the magnitude of the effects of concentrated ambient particles on heart function and morphology, as shown by increased HRV (heart rate variability), decreased heart rate and increased volume of connective tissue in left ventricle myocardium. LVH rats presented similar outcomes but more severe effects on the heart which included decreased blood pressure and increased cardiomyocyte hypertrophy compared to non-exposed LVH rats. In conclusion, our results corroborate with previous findings that particulate air pollution induces changes in the autonomic control of the heart and that individual with previous cardiovascular disease are more affected than normal ones. We have further shown that concentrated ambient particles are capable of inducing changes in the microstructure of the myocardium depending on accumulated dose of exposure. SUMÁRIO Lista de quadros

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Influência do tempo de exposição à obesidade sobre a expressão gênica e protéica do sistema regulador do trânsito de cálcio miocárdico

Leopoldo¹

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+2Dedico este trabalho às pessoas mais importantes da minha vida, À toda minha famíliaQue soube compreender todos os momentos em que estive ausente, obrigada pelos constantes incentivos e torcida pelo meu futuro. Vocês são essenciais! Aos meus PaisSignificado de devoção e coragem, com o exemplo deles, aprendi que tudo é possível com força de vontade e pensamento positivo, e, sobretudo, a importância da dignidade e do caráter. Amor eterno! Ao meu marido, André, Pelo privilégio de ter você ao meu lado, sempre carinhoso, otimista e compreensivo até nos momentos mais difíceis. Pelos momentos de esperança que pensa, junto comigo, no nosso futuro. Amo você! Há três coisas fundamentais para a felicidade:alguma coisa para fazer, alguém para amar e algo para esperar. Joseph Addison AGRADECIMENTOS ESPE AGRADECIMENTOS ESPE AGRADECIMENTOS ESPE AGRADECIMENTOS ESPECIAIS CIAIS CIAIS CIAISAo meu orientador, Prof. Dr. Antonio Carlos Cicogna, pela oportunidade, credibilidade e por ter me ensinado que ciência não se faz em poucas horas, mas sim em investigação científica baseada na observação e experimentação, com perseverança e muita dedicação. ABSTRACTCurrently, greater than one billion people are overweight and 30% of the population is obese.Several structural and functional changes of the heart have often been associated with human obesity. Experimental models for high-fat diets have been used to study the relationship between obesity and the heart. Myocardial calcium (Ca 2+ ) handling has been extensively studied in several experimental models and has often been shown to be related to cardiac dysfunction. However, few studies have evaluated the relationship between the duration of exposure to obesity and a high-fat diet, and mRNA and proteins involved in homeostasis of myocardial Ca 2+ . Some studies have reported the influence of thyroid hormones on these proteins, which may cause changes in cardiac contraction and relaxation. The main objective of the current study was to test the hypothesis that the increased duration of exposure to obesity leads to a reduction in the expression and/or phosphorylation of proteins and mRNA levels related to myocardial Ca 2+ handling. This study had, as additional objective, to verify if the decrease in mRNA expression was accompanied by a reduction in thyroid hormone levels.The periods of exposure to a high-fat diet used in this study were effective in promoting obesity since the adiposity index used to characterize animals as obese was 79.5%, 82%, and 69.5% higher than controls after 15, 30, and 45 weeks, respectively. The duration of exposure to a high-fat diet did not change the total body fat between the obese groups. This result indicates that there was not an increase in the intensity of obesity over time. In this study, some co-morbidities often associated with experimental obesity existed, such as glucose intolerance, insulin resistance, hyperinsulinemia, hyperleptinemia, and dyslipidemia; however, the co-morbidities were not associated with changes in systolic blood pressure.Obesi...

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Caracterização funcional da hipertrofia miocárdica induzida pelo isoproterenol e de sua regressão

Cited by 3 publications

References 25 publications

Isoproterenol‐Induced Hypertrophy May Result In Distinct Left Ventricular Changes

Isoproterenol‐Induced Hypertrophy May Result In Distinct Left Ventricular Changes

Efeitos cardiopulmonares da exposição ao material particulado fino (MP2,5) proveniente do concentrador de partículas ambientais (CPA) na hipertrofia ventricular esquerda de ratos wistar

Influência do tempo de exposição à obesidade sobre a expressão gênica e protéica do sistema regulador do trânsito de cálcio miocárdico

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