Steady-state Action Potential Duration Research Articles

Interaction of acidosis and increased extracellular potassium on action potential characteristics and conduction in guinea pig ventricular muscle.

We studied the individual and combined effects of extracellular acidosis and increases in extracellular potassium on action potential characteristics and conduction in order to gain a better understanding of the effects of acute ischemia. At each level of potassium between 2.7 and 17 mm, acidosis induced by increasing Pco2 (respiratory acidosis) and by decreasing HCO3- (metabolic acidosis) decreased resting membrane potential, the maximum rate of rise of the action potential upstroke (Vmax), and slowed conduction. Metabolic acidosis consistently and significantly lengthened the steady state action potential duration whereas respiratory acidosis did not. Respiratory acidosis caused changes in resting membrane potential, Vmax, and conduction velocity; which occurred more rapidly and were of greater magnitude than the changes induced by metabolic acidosis. The changes in Vmax induced both types of acidosis were due to a change in the resting membrane potential-Vmax relationship as well as to the changes in the resting membrane potential. The conduction slowing induced by acidosis was greater when potassium was 9 and 13 mM than when potassium was 5.4 mm. Our results suggest that acidosis causes important changes in the electrophysiological properties of ventricular fibers and that many of the known electrophysiological effects of acute ischemia can be mimicked by the combined effects of extracellular acidosis and an increase in extracellular potassium.

Effect of tetraethylammonium chloride on action potential in cardiac Purkinje fibers.

Intracellular loading with 20 mM tetraethylammonium chloride (TEA) diffusing through the cut end of the preparations prolonged action potential duration (APD) in dog Purkinje fibers without changing maximum diastolic potential, overshoot, and dV/dtmax. The APD was prolonged at all rates of stimulation, but, contrary to the normal rules, APD increased more after longer than after shorter interstimulus intervals. TEA increased the number of beats required to achieve the new steady-state APD after an abrupt change in the rate of stimulation. The effect of varying extracellular potassium concentration on maximal diastolic potential suggested that intracellular loading with TEA had no effect on the time-independent "background" outward current (IK1). If we ascribe all observed TEA effects to the reduction of time dependent slow outward current Ix1, we can propose a hypothesis concerning the role of Ix1 in the regulation of APD at slow heart rates.