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1Instituto de Investigaciones Cardiológicas, School of Medicine (Universidad de Buenos Aires-Consejo Nacional de Investigaciones Cientificas y Técnicas) and 2Biophysical Department, School of Dentistry, Universidad de Buenos Aires, 1122, Buenos Aires, Argentina; and 3Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, 21949-900 Rio de Janeiro, Brazil
Submitted 8 December 2003 ; accepted in final form 3 May 2004
Chagasic (Ch) and nonchagasic (NCh) IgG fraction (20 µg/ml) effects on cardiac performance of adult Wistar rat ventricles were studied with a novel approach applying a microcalorimetric technique. Resting heat (Hr) was significantly decreased by Ch antibodies (
HrCh = 4.8 ± 0.9 mW/g). Although the Hr decrease can be associated with diminished activity of the Na+/K+ pump, the magnitude of the effect (25% of control Hr) indicates that additional processes may also be affected. Ch antibodies induced an initial increase in developed pressure (P), which was associated with a decreased contractile economy. However, after 30 min of Ch antibody perfusion, P reached a significantly lower level (
PCh = 3.8 ± 1.2 mN/mm2) without changes in active heat per beat (Ha). Consequently, Ha/P ratio increased, indicating that the energetic cost per unit of P was higher. In contrast, P and Ha were both significantly and reversibly decreased by NCh antibodies (
PNCh = 4.4 ± 1.2 mN/mm2;
HaNCh = 9.7 ± 2.2 mJ/g), but Ha/P remained unaffected. According to these data, normal hearts exposed to Ch antibodies present a biphasic mechanical response: 1) an initial period of increased contractility (and decreased global muscle economy) consistent with antibodies with
1-adrenergic activity, such as those used in the present study, and 2) a decrease in P at 30 min of Ch antibody perfusion, which suggests that another Ca2+-related mechanism is compromised. These data contribute to redefine the role of antibody-mediated responses in the pathophysiology of chronic chagasic cardiomyopathy as agents of myocardial failure.
cardiomyopathy; energy metabolism; ventricular function; muscle economy; excitation-contraction coupling
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