Cardiomyocyte dysfunction during the chronic phase of Chagas disease.

Danilo Roman-Campos,Hugo Leonardo Duarte,Catherine Ropert,Jader Santos Cruz,Silvia Guatimosim,Eneas Ricardo Gomes,Policarpo Sales-Júnior,Ricardo Tostes Gazzinelli

doi:10.1590/0074-0276108022013019

Abstract

Chagas disease, which is caused by the parasite Trypanosoma cruzi, is an important cause of heart failure. We investigated modifications in the cellular electrophysiological and calcium-handling characteristics of an infected mouse heart during the chronic phase of the disease. The patch-clamp technique was used to record action potentials (APs) and L-type Ca2+ and transient outward K+ currents. [Ca2+]i changes were determined using confocal microscopy. Infected ventricular cells showed prolonged APs, reduced transient outward K+ and L-type Ca2+ currents and reduced Ca2+ release from the sarcoplasmic reticulum. Thus, the chronic phase of Chagas disease is characterised by cardiomyocyte dysfunction, which could lead to heart failure.

Highlights

Chagas disease, which is caused by infection with the protozoan parasite Trypanosoma cruzi, is one of the leading causes of heart failure in Latin America (MarinNeto et al 2007)
Ca2+ imaging was performed in Fluo-4 AM (10 μM)-loaded cardiomyocytes that were stimulated at 1 Hz using a Zeiss LSM 510 META confocal microscope equipped with an argon laser (488 nm) and a 63X oil immersion objective in line-scan mode (Roman-Campos et al 2010)
To study the cellular mechanism of cardiomyocyte dysfunction during the chronic phase of Chagas disease, in which T. cruzi is no longer observed in the bloodstream (Roman-Campos et al 2009b), we first measured the transmembrane action potentials (APs) of cardiomyocytes isolated from online | memorias.ioc.fiocruz.br

Summary

Introduction

Chagas disease, which is caused by infection with the protozoan parasite Trypanosoma cruzi, is one of the leading causes of heart failure in Latin America (MarinNeto et al 2007). Until now, few studies have provided compelling evidence of cardiomyocyte dysfunction during the establishment of heart failure following infection by T. cruzi (de Carvalho et al 1992, Pacioretty et al 1995, Roman-Campos et al 2009b).

Results

Conclusion