Improved systolic ventricular function with normal myocardial mechanics in compensated cardiac hypertrophy

There is still controversy about the relation between changes in myocardial contractile function and global left ventricular (LV) performance during stable concentric hypertrophy. To clarify this, we analyzed LV function in vivo and myocardial mechanics in vitro in rats with pressure overload-induced cardiac hypertrophy. Male Wistar rats (70 g) Underwent ascending aortic stenosis for 8 weeks (group AAS, n = 9). LV performance wits assessed by transthoracic echocardiography Under anesthesia. Myocardial function Was studied in isolated papillary muscle preparations during isometric contraction. The data were compared with age- and sex-matched sham-operated rats (group C, 11 = 9). LV weight-to-body weight ratio (C: 2.13 +/- 0.14 mg/g; AAS: 3.24 +/- 0.44) LV relative wall thickness (C: 0.18 +/- 0.02; AAS: 0.33 +/- 0.09), and LV fractional shortening (C: 54 +/- 5%; AAS: 70 +/- 8%) were increased in group AAS (P<0.05). Echocardio-graphic analysis also indicated a significant association (r = 0.74 P<0.001) between the percent fractional shortening index and LV relative wall thickness. The performance of AAS isolated In muscle revealed that active tension (C: 6.6 +/- 1.7 g/mm(2); AAS: 6.5 +/- 1.5 g/mm(2)) and maximum rate of tension development (C: 69 +/- 21 g/mm(2)/s AAS: 69 +/- 18 g/mm(2)/s) were not significantly different Front group C (P>0.05). In conclusion, compensated pressure-overload myocardial hypertrophy is associated with preserved myocardial function and increased ventricular performance. The improved LV function might be due to the ventricular remodeling, characterized by an increased relative wall thickness.

Calorimetry, Morphometry, Oxidative Stress, and Cardiac Metabolic Response to Growth Hormone Treatment in Obese and Aged Rats

This study investigated the effects of growth hormone therapy on energy expenditure, lipid profile, oxidative stress and cardiac energy metabolism in aging and obesity conditions. Life expectancy is increasing in world population and with it, the incidence of public health problems such as obesity and cardiac alterations. Because growth hormone (GH) concentration is referred to be decreased in aging conditions, a question must be addressed: what is the effect of GH on aging related adverse changes? To investigate the effects of GH on cardiac energy metabolism and its association with calorimetric parameters, lipid profile and oxidative stress in aged and obese rats, initially 32 male Wistar rats were divided into 2 groups (n = 16), C: given standard-chow and water; H: given hypercaloric-chow and receiving 30 % sucrose in its drinking water. After 45 days, both C and H groups were divided into 2 subgroups (n = 8), C + PL: standard-chow, water, and receiving saline subcutaneously; C + GH: standard-chow, water, and receiving 2 mg/kg/day rhGH subcutaneously; H + PL: hypercaloric-chow, 30 % sucrose, receiving saline subcutaneously; H + GH: hypercaloric-chow, 30 % sucrose, receiving rhGH subcutaneously. After 30 days, C + GH and H + PL rats had higher body mass index, Lee-index, body fat content, percent-adiposity, serum triacylglycerol, cardiac lipid-hydroperoxide, and triacylglycerol than C + PL. Energy-expenditure (RMR)/body weight, oxygen consumption and fat-oxidation were higher in H + GH than in H + PL. LDL-cholesterol was highest in H + GH rats, whereas cardiac pyruvate-dehydrogenase and phosphofrutokinase were higher in H + GH and H + PL rats than in C + PL. In conclusion, the present study brought new insights on aging and obesity, demonstrating for the first time that GH therapy was harmful in aged and obesity conditions, impairing calorimetric parameters and lipid profile. GH was disadvantageous in control old rats, having undesirable effects on triacylglycerol accumulation and cardiac oxidative stress.

Swimming training exacerbates pathological cardiac hypertrophy in kinin B(2) receptor-deficient mice

Kallikrein-kinin system exerts cardioprotective effects against pathological hypertrophy. These effects are modulated mainly via B(2) receptor activation. Chronic physical exercise can induce physiological cardiac hypertrophy characterized by normal organization of cardiac structure. Therefore, the aim of this work was to verify the influence of kinin B(2) receptor deletion on physiological hypertrophy to exercise stimulus. Animals were submitted to swimming practice for 5 min or for 60 min, 5 days a week, during 1 month and several cardiac parameters were evaluated. Results showed no significantly difference in heart weight between both groups, however an increased left ventricle weight and myocyte diameter were observed after the 60 min swimming protocol, which was more pronounced in B(2)(-/-) mice. In addition, sedentary B(2)(-/-) animals presented higher left ventricle mass when compared to wild-type (WT) mice. An increase in capillary density was observed in exercised animals, however the effect was less pronounced in B(2)(-/-) mice. Collagen, a marker of pathological hypertrophy, was increased in B(2)(-/-) mice submitted to swimming protocol, as well as left ventricular thickness, suggesting that these animals do not respond with physiological hypertrophy for this kind of exercise. In conclusion, our data suggest an important role for the kinin B(2) receptor in physiological cardiac hypertrophy. (c) 2007 Elsevier B.V. All rights reserved.

Cardiac benefits of exercise training in aging spontaneously hypertensive rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Disposable immunosensor for human cardiac troponin T based on streptavidin-microsphere modified screen-printed electrode

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Energy Expenditure and Oxygen Consumption as Novel Biomarkers of Obesity-induced Cardiac Disease in Rats

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Conjugated linoleic acid and cardiac health: Oxidative stress and energetic metabolism in standard and sucrose-rich diets

Studies on conjugated linoleic acid ingestion and its effect on cardiac tissue are necessary for the safe utilization of this compound as supplement for weight loss. Male Wistar 24-rats were divided into four groups (n = 6):(C)given standard chow, water and 0.5 ml saline, twice a week by gavage; (C-CLA)receiving standard chow, water and 0.5 ml of conjugated linoleic acid, twice a week, by gavage; (S)given standard chow, saline by gavage, and 30% sucrose in its drinking water; (S-CLA)receiving standard chow, 30% sucrose in its drinking water and conjugated linoleic acid. After 42 days of treatment S rats had obesity with increased abdominal-circumference, dyslipidemia, oxidative stress and myocardial lower citrate synthase(CS) and higher lactate dehydrogenase(LDH) activities than C. Conjugated linoleic acid had no effects on morphometric parameters in C-CLA, as compared to C, but normalized morphometric parameters comparing S-CLA with S. There was a negative correlation between abdominal adiposity and resting metabolic rate. Conjugated linoleic acid effect, enhancing fasting-VO2/surface area, postprandial-carbohydrate oxidation and serum lipid hydroperoxide resembled to that of the S group. Conjugated linoleic acid induced cardiac oxidative stress in both fed conditions, and triacylglycerol accumulation in S-CLA rats. Conjugated linoleic acid depressed myocardial LDH comparing C-CLA with C, and beta-hydroxyacyl-coenzyme-A dehydrogenase/CS ratio, comparing S-CLA with S. In conclusion, dietary conjugated linoleic acid supplementation for weight loss can have long-term effects on cardiac health. Conjugated linoleic acid, isomers c9, t11 and t10, c12 presented undesirable pro-oxidant effect and induced metabolic changes in cardiac tissue. Nevertheless, despite its effect on abdominal adiposity in sucrose-rich diet condition, conjugated linoleic acid may be disadvantageous because it can lead to oxidative stress and dyslipidemic profile. (c) 2007 Elsevier B.V All rights reserved.