TY - JOUR
T1 - Conduction Defects and Arrhythmias in Chagas' Disease
T2 - Possible Role of Gap Junctions and Humoral Mechanisms
AU - DE CARVALHO, ANTONIO C.CAMPOS
AU - MASUDA, MASAKI O.
AU - TANOWITZ, HERBERT B.
AU - WITTNER, MURRAY
AU - GOLDENBERG, REGINA C.S.
AU - SPRAY, DAVID C.
PY - 1994/8
Y1 - 1994/8
N2 - 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.
AB - 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.
KW - Trypanosoma cruzi
KW - connexin
KW - heart
KW - immunity
KW - parasite
UR - http://www.scopus.com/inward/record.url?scp=0027958785&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027958785&partnerID=8YFLogxK
U2 - 10.1111/j.1540-8167.1994.tb01191.x
DO - 10.1111/j.1540-8167.1994.tb01191.x
M3 - Review article
C2 - 7804521
AN - SCOPUS:0027958785
SN - 1045-3873
VL - 5
SP - 686
EP - 698
JO - Journal of cardiovascular electrophysiology
JF - Journal of cardiovascular electrophysiology
IS - 8
ER -