Isolated obesity resistance condition or associated with aerobic exercise training does not promote cardiac impairment.

Mechanisms involved in cardiac function and calcium (Ca2+) handling in obese-resistant (OR) rats are still poorly determined. We tested the hypothesis that unsaturated high-fat diet (HFD) promotes myocardial dysfunction in OR rats, which it is related to Ca2+ handling. In addition, we questioned whether exercise training (ET) becomes a therapeutic strategy. Male Wistar rats (n=80) were randomized to standard or HFD diets for 20 weeks. The rats were redistributed for the absence or presence of ET and OR: control (C; n=12), control + ET (CET; n=14), obese-resistant (OR; n=9), and obese-resistant + ET (ORET; n=10). Trained rats were subjected to aerobic training protocol with progressive intensity (55-70% of the maximum running speed) and duration (15 to 60 min/day) for 12 weeks. Nutritional, metabolic, and cardiovascular parameters were determined. Cardiac function and Ca2+ handling tests were performed in isolated left ventricle (LV) papillary muscle. OR rats showed cardiac atrophy with reduced collagen levels, but there was myocardial dysfunction. ET was efficient in improving most parameters of body composition. However, the mechanical properties and Ca2+ handling from isolated papillary muscle were similar among groups. Aerobic ET does not promote morphological and cardiac functional adaptation under the condition of OR.

Calcium homeostasis behavior and cardiac function on left ventricular remodeling by pressure overload.

Sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) and sarcolemmal Na+/Ca2+ exchanger (NCX1) structures are involved in heart cell Ca2+ homeostasis. Previous studies have shown discrepancies in their function and expression in heart failure. The goal of this study was to evaluate heart function and hypertrophied muscle Ca2+-handling protein behavior under pressure overload. Twenty male Wistar rats were divided into two groups: Aortic stenosis (AoS), induced by a clip placed at the beginning of the aorta, and Control (Sham). After 18 weeks, heart function and structure were evaluated by echocardiogram. Myocardial function was analyzed by isolated papillary muscle (IPM) at basal condition and Ca2+ protein functions were evaluated after post-pause contraction and blockage with cyclopiazonic acid in IPM. Ca2+-handling protein expression was studied by western blot (WB). Echocardiogram showed that AoS caused concentric hypertrophy with enhanced ejection fraction and diastolic dysfunction inferred by dilated left atrium and increased relative wall thickness. IPM study showed developed tension was the same in both groups. AoS showed increased stiffness revealed by enhanced resting tension, and changes in Ca2+ homeostasis shown by calcium elevation and SERCA2a blockage maneuvers. WB revealed decreased NCX1, SERCA2a, and phosphorylated phospholambam (PLB) on serine-16 in AoS. AoS had left ventricular hypertrophy and diastolic dysfunction compared to Sham; this could be related to our findings regarding calcium homeostasis behavior: deficit in NCX1, SERCA2a, and phosphorylated PLB on serine-16.

Isolated obesity resistance condition or associated with aerobic exercise training does not promote cardiac impairment

Mechanisms involved in cardiac function and calcium (Ca2+) handling in obese-resistant (OR) rats are still poorly determined. We tested the hypothesis that unsaturated high-fat diet (HFD) promotes myocardial dysfunction in OR rats, which it is related to Ca2+ handling. In addition, we questioned whether exercise training (ET) becomes a therapeutic strategy. Male Wistar rats (n=80) were randomized to standard or HFD diets for 20 weeks. The rats were redistributed for the absence or presence of ET and OR: control (C; n=12), control + ET (CET; n=14), obese-resistant (OR; n=9), and obese-resistant + ET (ORET; n=10). Trained rats were subjected to aerobic training protocol with progressive intensity (55-70% of the maximum running speed) and duration (15 to 60 min/day) for 12 weeks. Nutritional, metabolic, and cardiovascular parameters were determined. Cardiac function and Ca2+ handling tests were performed in isolated left ventricle (LV) papillary muscle. OR rats showed cardiac atrophy with reduced collagen levels, but there was myocardial dysfunction. ET was efficient in improving most parameters of body composition. However, the mechanical properties and Ca2+ handling from isolated papillary muscle were similar among groups. Aerobic ET does not promote morphological and cardiac functional adaptation under the condition of OR.

Calcium homeostasis behavior and cardiac function on left ventricular remodeling by pressure overload

Sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) and sarcolemmal Na+/Ca2+ exchanger (NCX1) structures are involved in heart cell Ca2+ homeostasis. Previous studies have shown discrepancies in their function and expression in heart failure. The goal of this study was to evaluate heart function and hypertrophied muscle Ca2+-handling protein behavior under pressure overload. Twenty male Wistar rats were divided into two groups: Aortic stenosis (AoS), induced by a clip placed at the beginning of the aorta, and Control (Sham). After 18 weeks, heart function and structure were evaluated by echocardiogram. Myocardial function was analyzed by isolated papillary muscle (IPM) at basal condition and Ca2+ protein functions were evaluated after post-pause contraction and blockage with cyclopiazonic acid in IPM. Ca2+-handling protein expression was studied by western blot (WB). Echocardiogram showed that AoS caused concentric hypertrophy with enhanced ejection fraction and diastolic dysfunction inferred by dilated left atrium and increased relative wall thickness. IPM study showed developed tension was the same in both groups. AoS showed increased stiffness revealed by enhanced resting tension, and changes in Ca2+ homeostasis shown by calcium elevation and SERCA2a blockage maneuvers. WB revealed decreased NCX1, SERCA2a, and phosphorylated phospholambam (PLB) on serine-16 in AoS. AoS had left ventricular hypertrophy and diastolic dysfunction compared to Sham; this could be related to our findings regarding calcium homeostasis behavior: deficit in NCX1, SERCA2a, and phosphorylated PLB on serine-16.

Biosensor de ácido úrico para determinaçäo em fluxo contínuo / Uric acid biosensor for continuous flow determination

O objetivo deste trabalho foi desenvolver um biosensor para dosagens de ácido úrico no soro humano. A uricase foi imobilizada em pasta de grafite modificada usando TCNQ como mediador e então, pressionada sobre um eletrodo de outo. A corrente elétrica produzida pela reação enzimática foi diretamente proporcional à concentração de ácido úrico presente na amostra. Este sistema demonstrou uma sensibilidade linear entre 12.5 muM a 250 muM de solução de ácido úrico. O sistema foi testado usando medições em fluxo contínuo (FIA).

The aim of this work was to develop a biosensor to determine uric acid concentration in human serum. Uricase was immobilized in modified graphite paste using TCNQ as a mediator and then packed onto a gold electrode. The current produced by the enzyme reaction was proportional to the uric acid concentration in the sample. The response of this system showed a linear sensivity between concentrations of 12.5 µM and 250 ~tM uric acid solutions. The system was tested using flow injection analysis (FIA).