Reduction of the transient outward potassium current in a canine model of Chagas' disease.

The effects of Chagas' disease, an important cause of cardiac arrhythmias and cardiomyopathy, on cellular electrical properties were determined in epicardial tissue from normal dogs and dogs infected with Trypanosoma cruzi for 20-25 days (25 DPI), at the time of maximum parasitemia, and for 125-140 days (140 DPI) after the parasitemia had subsided. At 25 DPI, phase 1 repolarization of the action potential was attenuated and the transient outward current (Ito) was reduced from 10.2 +/- 0.5 to 5.5 +/- 0.6 pA/pF. No differences were apparent between infected and normal cells in the time constants of current decay (25.6 +/- 4.0 and 22.8 +/- 1.3 ms, respectively) or in the steady-state inactivation parameters (V1/2 = -34.1 +/- 3.6 and -34.6 +/- 1.4 mV and k = 6.3 +/- 1.8 and 4.0 +/- 0.3, respectively). The rapid phase of recovery from inactivation was nearly eliminated in infected myocytes, whereas the slower phase was unaffected. Phase 1 repolarization and Ito density at 140 DPI were not significantly different from normal cells. Thus T. cruzi acutely inhibited Ito in epicardial myocytes, an effect that was reversed with abatement of the parasitemia.