Exposição ao chumbo por 30 dias: implicações na pressão arterial e na contratilidade miocárdica

• Autor(a) principal: Fioresi, Mirian
• Data de Publicação: 2011
• Tipo de documento: Tese
• Idioma: por
• Título da fonte: Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)
• Texto Completo: http://repositorio.ufes.br/handle/10/8043
• topic: Fisiologia; 612

The aim of this study was to investigate the cardiovascular effects of exposure to lead for 30 days, emphasizing its direct action on myocardial contractility. Male Wistar rats were sorted randomly into two groups: control (Ct) and treated with 100 ppm of lead in drinking water (Pb). Blood pressure (BP) was measured weekly. At the end of treatment, animals were anesthetized and hemodynamic parameters were measured. After this procedure the rats were sacrificed for myocardial contractility assessment, in vitro. Blood and tissue samples were properly stored for further biochemical investigation. Statistical analysis: mean ± SEM; one or two-way ANOVA or Student's t-test were used. p <0.05 was considered significant. The blood concentration of lead in the treated group was approximately 13 mg/dL, below the maximum allowable biological index in Brazil (60 mg/dL) and bone showed to be the site of highest deposition of this metal. The BP in Pb group was higher than the Ct group since the first week of exposure to lead and remained like that over the next four weeks. Hemodynamic evaluation, at 30 days, showed an increase in systolic blood pressure (Ct: 96 ± 3.79 vs. Pb: 116 ± 1.37 mmHg), diastolic (Ct: 60 ± 2.93 vs. Pb: 70 ± 3.38 mmHg), left ventricular (Ct: 104 ± 5.85 vs. Pb: 120 ± 2.51 mmHg) and heart rate (Ct: 307 ± 10 vs. Pb: 348 ± 16 bpm). In vitro, lead treatment did not change the inotropic state (contraction force and time derivatives of force). However, our results are suggestive of changes in the kinetics of calcium (Ca++) in the cardiomyocyte. These changes are explained by the increased transarcolemmal Ca++ influx, associated with the lower Ca++ uptake by the sarcoplasmic reticulum and high extrusion by sarcolemma. Altogether, these results show that despite the increased Ca++ influx induced by lead, the myocyte had regulatory mechanisms that prevent the increase of force, as seen in vivo. Our work has shown that lead exposure results in high blood pressure as well as increase on HR and ventricular inotropism. In addition, it showed for the first time, that lead exposure causes changes in the calcium cycle of cardiomyocytes. Such changes may contribute to the deleterious effects of this metal on the cardiovascular system.