Efeitos da exposição aguda ao acetato de chumbo sobre os parâmetros cardiovasculares de ratos

• Ano de defesa: 2008
• Autor(a) principal: Fioresi, Mirian
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal do Espírito Santo; BR; Mestrado em Ciências Fisiológicas; Centro de Ciências da Saúde; UFES; Programa de Pós-Graduação em Ciências Fisiológicas
• Palavras-chave em Português: Chumbo; Hemodinâmica; Músculo isolado; Ratos; Fisiologia; 612
• Link de acesso: http://repositorio.ufes.br/handle/10/7915

Several studies in human population and animal models demonstrated a correlation between the Pb++ blood concentration and arterial pressure. However, studies that evaluate cardiac effects resulting from the exposure to this metal are still scarce. Considering the lack of studies about lead effects on the cardiac contractility the objective of this work was to study the cardiovascular effects of the acute exposure of this metal in rats. Wistar rats (280 to 350 g) were used to perform hemodynamic studies (ventricular performance in vivo), cardiac contractility and biochemical parameters. Rats were anesthetized and the left (LV) and right ventricle (RV) catheterized to measure the following parameters during 120 minutes exposure to lead acetate (80 µg/dL): LV systolic pressure (SP), positive (+) and negative (-) time derivative of ventricular pressure (dP/dt) and heart rate (HR). Cardiac contractility was evaluated with LV papillary muscles. For that we measured: cardiac inotropic responses, temporal parameters, the sarcoplasmic reticulum activity and the sarcolemmal permeability to calcium and the role of contractile proteins. All measures were undertaken before and after the acute exposure to 8 µM lead acetate. The specific activities of the cardiac Na+ -K+ -ATPase (NKA) and myosin Ca2+ ATPase were also measured in samples exposed or not to 8 µM Pb++ . Results are presented as mean ± SEM and analyzed by: one-way ANOVA or Student t-test. p < 0,05 was considered significant. The exposure to Pb++ for 2 hours produced a significant increase of the measured parameters in LV and RV (LV and RV: SP, dP/dt +, dP/dt-). However, no significant change of HR was observed. The study of contractile parameters in vitro showed in positive inotropic effect after the acute lead exposure. Regarding the time parameters of the isometric contraction of papillary muscles there was a reduction of time to peak tension but the relaxation time did not change as well as the sarcoplasmic reticulum activity. After 1 hour of lead exposure the papillary muscles became hyperreactive to a β-adrenergic agonist. Also, the results of post-rest contractions were suggestive of a reduction of sarcolemmal calcium influx. Biochemical analyses showed that myocardial samples treated with 8µM Pb++ showed an increase of the NKA ATPase and myosin ATPase activities compared to the untreated samples. The reduction of the calcium influx could reduce the force production in cardiac myocytes and, consequently, reduce inotropism. However, against this fact, there was an increase of cardiac inotropism both in isolated muscles as in in vivo. Then, if the acute exposure to lead produces some deleterious effect, capable to reduce myocardial force development, this effect was counteracted and exceed by the activation of other compensatory mechanisms: increase of myosin ATPase activity; neuroendocrine changes (increase of sympathetic tone), or changes in the transductional mechanisms (mimic of Ca++ by Pb++ in the contractile activation). In conclusion, our work showed, by the first time, that the increase of ventricular pressure induced by lead have, beyond the vascular involvement, direct changes in the myocardial contractility