108 resultados para heart ventricle hypertrophy
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Pós-graduação em Ciência Animal - FMVA
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Pós-graduação em Fisiopatologia em Clínica Médica - FMB
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Pós-graduação em Fisiopatologia em Clínica Médica - FMB
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Objectives: This experimental study aimed to evaluate the effects of central catalase inhibition on cardiovascular responses in rats exposed to sidestream cigarette smoke (SSCS) for 3 weeks. Methodology: A total of 20 males Wistar rats (320–370g) were implanted with a stainless steel guide cannula into the fourth cerebral ventricle (4thV). Femoral artery and vein were cannulated for mean arterial pressure (MAP) and heart rate (HR) measurement and drug infusion, respectively. Rats were exposed to SSCS for three weeks, 180 minutes per day, 5 days/week [carbon monoxide (CO): 100–300 ppm)]. Baroreflex was tested with one pressor dose of phenylephrine (PHE, 8 μg/kg, bolus) and one depressor dose of sodium nitroprusside (SNP, 50 μg/kg, bolus). Cardiovascular responses were evaluated before and 15 minutes after 3-amino-1, 2, 4-triazole (ATZ, catalase inhibitor, 0.001g/100μL) injection into the 4th V. Results: Vehicle treatment into the 4th V did not change cardiovascular responses. Central catalase inhibition increased tachycardic peak, attenuated bradycardic peak and reduced HR range at 15 minutes, increased MAP at 5, 15 and 30 min and increased HR at 5 and 15 min. In rats exposed to SSCS, central ATZ increased basal MAP after 5 min and increased HR at 5, 15 and 30 minutes, respectively, and attenuated bradycardic peak at 15 minutes. Conclusion: This study suggests that brain oxidative stress caused by SSCS influences autonomic regulation of the cardiovascular system.
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Aortic regurgitation (AR) leads to a left ventricle dilation and hypertrophy in response to a chronic volume overload. It is still very frequent in developing countries, for instance Brazil, and often as secondary to rheumatic fever. Usually, chronic AR is generally well tolerated for many years, when with the heart dilated the patient searches for treatment. Bidirectional association with depression and cardiovascular disease has been described. Selective serotonin reuptake inhibitors (SSRI) are widely prescribed to treat several affective disorders, especially for cardiovascular patients since they decrease arrhythmia probability. These SSRI improves cardiac function in rats submitted to stress protocols. Preliminary study from our laboratory showed that following 4 weeks of treatment with one SSRI (paroxetine) in subchronic AR rats there was a decreased in daily sodium intake and an improvement in systolic function. An increase in the central oxytocinergic transmission may be involved in this peripheral improvement to the heart. The investigations about the mechanisms underlying this improvement are necessary. Therefore the aims of this project is investigate the effects of 4 weeks of treatment of paroxetine, a SSRI, in rats with a subchronic AR over the central central gene expression of oxytocin and vasopressin using a reverse transcription polymerase chain reaction (RT-PCR)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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In renovascular hypertensive rats, low doses of angiotensin converting enzyme (ACE) inhibitors have been found to prevent myocardial hypertrophy independent of blood pressure level. This finding would suggest humoral rather than mechanical control of myocyte growth. The aim of this study was to examine the effect of nonantihypertensive doses of ACE inhibitor on myocardial hypertrophy and necrosis in hypertensive rats. Renovascular hypertension (RHT) was induced in four-week-old Wistar rats. Twenty-eight animals were treated for four weeks with three doses of ramipril (0.01, 0.1 or 1. 0 mg/kg/day, which are unable to lower blood pressure. Fourteen animals were not treated (RHT group). A sham operated, age/sex-matched group was used as control (n = 10). Myocardial histology was analysed in 3 microm thick sections of the ventricle stained with either haematoxylin-eosin, reticulin silver stain or Masson's trichrome. There was a significant correlation between systolic blood pressure and left ventricular to body weight ratio in both sets of animals: untreated plus controls and ramipril-treated rats. ACE inhibition prevented myocyte and perivascular necrosis and fibrosis in a dose-dependent manner. We conclude that myocardial hypertrophy in rats with renovascular hypertension is directly related to arterial pressure, and that this relationship is not affected by nonantihypertensive doses of ACE inhibitor. Myocardial necrosis/fibrosis and coronary artery damage induced by angiotensin II are prevented by ACE inhibitor in a dose-dependent manner, despite the presence of arterial hypertension.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)