RESUMO
The p22-phox subunit is an essential component of NAD(P)H oxidase enzymatic complex, which is considered the major source of oxidative stress products in the cardiovascular system. The -930G allele of p22-phox has been associated with higher promoter activity, increased NAD(P)H oxidase-mediated oxidative stress and hypertension. We recently reported that left ventricular hypertrophy is accompanied by increased myocardial p22-phox expression in aortic-banded rats, suggesting that this protein might be involved in hypertensive cardiac hypertrophy.
Assuntos
Hipertensão/genética , Hipertensão/patologia , NADPH Oxidases/genética , Polimorfismo Genético , Adulto , Brasil , Feminino , Humanos , Hipertrofia Ventricular Esquerda/etiologia , Hipertrofia Ventricular Esquerda/genética , Rim/patologia , Masculino , Pessoa de Meia-Idade , Estresse Oxidativo , Regiões Promotoras GenéticasAssuntos
Equinococose/diagnóstico , Cardiopatias/diagnóstico , Albendazol/uso terapêutico , Animais , Anticestoides/uso terapêutico , Equinococose/tratamento farmacológico , Equinococose/cirurgia , Ecocardiografia Transesofagiana , Cardiopatias/tratamento farmacológico , Cardiopatias/cirurgia , Humanos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Radiografia TorácicaRESUMO
There is a paucity of experimental data on the actual mechanism of insulin-induced changes on the myocardial function. In the present study we investigated the myocardial contractile, response to an oral glucose load using echocardiography. Fifteen healthy volunteers were studied after overnight fast and 150 minutes after the oral load of 75 g glucose. Oral glucose load caused an increase in plasma glucose and insulin levels, which was accompanied by a significant increase in left ventricular shortening (from 35.2 +/- 0.7% at baseline, to 38.5 +/- 0.6% and 39 +/- 0.9% at 30 and 60 minutes post glucose load, respectively [P < 0.05 vs baseline]; ejection fraction rose from 0.73% +/- 0.01 to 0.77% +/- 0.01 (P < 0.05); pressure rate product increased from 7.29 +/- 0.2 to 8.31 +/- 0.3 mmHg x beats per min (P < 0.007) and heart rate enhanced from 68.3 +/- 1.9 to 74 +/- 1.6 (P < 0.034) and 75.3 +/- 1.5 beats per min (P < 0.008) at 60 and 90 minutes after glucose, respectively. Meanwhile, mean arterial pressure decreased significantly (10 +/- 1.5%, P < 0.018) when compared to basal values. These results indicate a significant change in the myocardial contractile response to an oral glucose load, probably related to baroreceptor reflex response as well as an overridden by a potent vasodilator action of insulin. Nevertheless, we could not rule out that the cardiac effects may also be due an insulin-induced sympathetic activation or a direct myocardial effect.