Gap Junctions and Humoral Factors in Chagas’ Disease. The protozoan parasite Trypanosoma cruzi causes Chagas’ disease, a major cause of cardiac dysfunction in Latin Americans. Chagas’ disease exhibits both acute and chronic phases, and each may be characterized by cardiac conduction disturbances. In acutely infected cultures of rodent heart cells, synchronized spontaneous beating becomes less regular, and coupling between cells is reduced. The basis of this decreased conduction is apparently in localization of the gap junction protein (Cx43) inside infected cells. Although total Cx43 is normal in infected cells, little is recognizable at appositional membranes. Electrophysiological properties are also altered by this infection. Action potentials are shortened, resting Ca2+ levels are elevated, and response to α‐adrenergic agonists was altered, compared to controls. Humoral factors may contribute to the conduction defects in chronic Chagas’ disease. Sera from chronically infected rabbits produced KC(J abnormalities in Langendorff‐perfused rabbit hearts. These findings indicate that chagasic infection may modify ion channel function in the heart, and we suggest that these changes may be manifested in the conduction disturbances that characterize this disease.
|Number of pages
|Journal of cardiovascular electrophysiology
|Published - Aug 1994
- Trypanosoma cruzi
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)