TEA prevents the decline of the duration of the action potential in hypoxic cardiac muscle.

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Our study was designed to evaluate the effects of the K+ channel blocker tetraethylammonium TEA (20 mM), Ca++ ionophore A23187 (6.9 μM), the Ca++ channel blocker verapamil (2 μM), and CaCl2 (6 mM) on a model of heart damage, hypoxia/reoxygenation of isolated guinea-pig hearts. The right ventricular papillary muscles maintained at 37°C and paced at 60 beats/min were perfused with Ringer solution equilibrated with 95% O2-5% CO2 (normoxia) or 95% N2-5% CO2 (hypoxia). After stabilization of the electrical and mechanical activity, 60 min of hypoxia was induced and then followed by 15 min of reoxygenation. During hypoxia, there was a significant decrease in the action potential duration (APD) and the contractile force (CF). The decrease in APD in the TEA-treated muscle was significantly less than that in the non-treated muscle. However, CF declined at the same rate in both groups. Neither A23187, CaCl2 nor verapamil prevented the decline in both APD and CF. To study the slow responses, the fast Na+ current was first voltage-inactivated by partial depolarization to about -40 mM using an elevated K+ solution. The rate of hypoxia-induced blockade of the slow response was not slower in the presence of 20 mM TEA. These data demonstrate that TEA significantly prevented the decline of APD in hypoxia, but this resistance in APD did not affect the rate of inhibition of mechanical activity.
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