Mechanical and energetic effects of chronic chagasic patients' antibodies on rat myocardium

• Published in: American journal of physiology. Heart and circulatory physiology 2004-09, Vol.56 (3), p.H1239-H1245
• Main Authors: SAVIO-GALIMBERTI, Eleonora, DOS SANTOS COSTA, Patricia, CAMPOS DE CARVALHO, Antonio Carlos, PONCE-HORNOS, Jorge Emilio
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Circulatory system; Fundamental and applied biological sciences. Psychology; Heart; Metabolism; Muscular system; Patients; Rodents; Vertebrates: cardiovascular system
• ISSN: 0363-6135; 1522-1539

Chagasic (Ch) and nonchagasic (NCh) IgG fraction (20 [micro]g/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 ({Delta}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 ({Delta}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 ({Delta}PNCh = 4.4 +/- 1.2 mN/mm2; {Delta}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 {beta}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. [PUBLICATION ABSTRACT]