RESUMO
This article describes the development and application of a new electrochemical methodology based on potential-modulated UV-vis reflectance spectroscopy (PMRS). The device configuration is based upon a thin-layer flow-through channel cell incorporating a platinum working electrode. Reagent solutions are pumped through the cell under well-defined hydrodynamic conditions and electrolyzed at the platinum working electrode. Measurements are presented for linear sweep and fixed dc potentials with a superimposed small amplitude sinusoidal potential perturbation. A UV-vis source is employed to irradiate the electrode region, and the resulting reflected signal is analyzed using a phase sensitive detector. Experimental studies using tris(4-bromophenyl) amine (TBPA) in acetonitrile are presented which quantify the relationship between the absorption spectrum and reflected light intensity as a function of the transport rate, electrolysis reactions, and the modulation frequency of the incident irradiation. The experimental results are analyzed using numerical simulations based on a finite difference strategy. These permit the quantitative prediction of the concentration distribution of reagents within the cell. A fast Fourier transform (FFT) routine was used to analyze the frequency response of the numerically predicted reflectance signal. Excellent agreement was observed between the numerical predictions and experimental observations.
RESUMO
In the model of myocardial infarction produced by occlusion of left anterior descending coronary artery (LAD) in rabbit, gypenosides (GP 100 but not 50 mg/kg, ip) reduced myocardial infarct size and decreased serum free fatty acid (FFA). In rat model of myocardial infarction, GP and the fractions of GP of non ginsenosides (FGNG) both in dose of 100 mg/kg, ip, protected significantly myocardial superoxide dismutase (SOD) activity and decreased the myocardial malondialdehyde (MDA). The results indicate that the protective effect of GP on myocardial infarction may be correlated with its prevention of myocardial lipid peroxidation, and attributed to the amelioration of FFA metabolic deterioration.
