Depressant effect of taurine on triggered activity induced by cesium chloride in rabbit hearts in vivo
Abstract
AIM:
To study the effects of taurine (Tau) and tetrodotoxin (Tet) on cesium chloride (CsCl)-induced triggered activity and arrhythmia in anesthetized rabbits.
METHODS:
With a cuffed endotracheal tube, the rabbit ventilation was maintained by a respirator. A Franzy's contact electrode catheter was advanced into the right ventricle through the right external jugular vein and positioned against the anteroapical endocardial surface to record the monophasic action potential (MAP). A catheter was placed into femoral vein for systemic drug administration.
RESULTS:
CsCl (1 mmol L-1 iv) produced a decrease in the amplitude of MAP from 42.2 +/- 2.1 to 37.0 +/- 3.8 mV (P < 0.01), a prolongation of MAPD50 (156 +/- 22 to 209 +/- 26 ms, P < 0.01) or MAPD90 (205 +/- 25 to 250 +/- 20 ms, P < 0.01) and an early afterdepolarization (EAD) developed within 30 s after CsCl injection. The ventricular premature (VP) resulted from EAD triggered by CsCl. In the Tau (100 mg kg-1)- or Tet (10 micrograms kg-1)-pretreated group, not only was the amplitude of EAD decreased (Tau, 4.2 +/- 2.7; or Tet, 5.2 +/- 2.6, respectively vs 16.1 +/- 8.3 mv, P < 0.01), but also the duration of EAD was shortened (Tau, 695 +/- 164; or Tet, 492 +/- 172, respectively, vs 1068 +/- 166 ms, P < 0.01). The severity of triggered arrhythmia (TA) was alleviated and the incidence of TA was lowered within 30 min after iv CsCl by either Tau or Tet.
CONCLUSION:
The depressant effects of Tau and Tet on EAD and VP induced by CsCl were involved in an increase of outward current or a decrease of an inward current.
Keywords:
To study the effects of taurine (Tau) and tetrodotoxin (Tet) on cesium chloride (CsCl)-induced triggered activity and arrhythmia in anesthetized rabbits.
METHODS:
With a cuffed endotracheal tube, the rabbit ventilation was maintained by a respirator. A Franzy's contact electrode catheter was advanced into the right ventricle through the right external jugular vein and positioned against the anteroapical endocardial surface to record the monophasic action potential (MAP). A catheter was placed into femoral vein for systemic drug administration.
RESULTS:
CsCl (1 mmol L-1 iv) produced a decrease in the amplitude of MAP from 42.2 +/- 2.1 to 37.0 +/- 3.8 mV (P < 0.01), a prolongation of MAPD50 (156 +/- 22 to 209 +/- 26 ms, P < 0.01) or MAPD90 (205 +/- 25 to 250 +/- 20 ms, P < 0.01) and an early afterdepolarization (EAD) developed within 30 s after CsCl injection. The ventricular premature (VP) resulted from EAD triggered by CsCl. In the Tau (100 mg kg-1)- or Tet (10 micrograms kg-1)-pretreated group, not only was the amplitude of EAD decreased (Tau, 4.2 +/- 2.7; or Tet, 5.2 +/- 2.6, respectively vs 16.1 +/- 8.3 mv, P < 0.01), but also the duration of EAD was shortened (Tau, 695 +/- 164; or Tet, 492 +/- 172, respectively, vs 1068 +/- 166 ms, P < 0.01). The severity of triggered arrhythmia (TA) was alleviated and the incidence of TA was lowered within 30 min after iv CsCl by either Tau or Tet.
CONCLUSION:
The depressant effects of Tau and Tet on EAD and VP induced by CsCl were involved in an increase of outward current or a decrease of an inward current.