Key result
Trypanosoma cruzi infection prolongs action potentials and reduces K+ and Ca2+ currents in mouse ventricular cells.
These mouse data should not yet influence Chagas management; leaves open mechanistic translation to human cardiomyopathy.
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.
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Roman‐Campos et al. (2013) studied Chagas disease. Trypanosoma cruzi infection vs. Uninfected cells was evaluated on Cellular electrophysiological and calcium-handling characteristics. Trypanosoma cruzi infection in mouse ventricular cells during the chronic phase of Chagas disease caused prolonged action potentials and reduced K+ and Ca2+ currents and Ca2+ release.
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