[Arrhythmogenesis of changes in cellular ionic environments: ischemia-induced increase in intracellular resistance and slow conduction].

Cardiac action potentials result from the influx of sodium and calcium ions and the efflux of potassium ions. In the ischemic myocardium, homeostasis of ionic environments are seriously disturbed, producing abnormalities in impulse generation and propagation. Conduction velocity of impulse is directly related to the maximum upstroke velocity of the action potential (Vmax) and inversely related to the intracellular resistance (r1). During ischemic events, Vmax decreases and r1 increases. These changes in Vmax and r1 greatly diminish the conduction velocity and can lead to the occurrence of various arrhythmias. To evaluate the role of the increase in r1 on conduction slowing in cardiac ischemia, we simultaneously measured the changes in Vmax, r1 and conduction velocity of the papillary muscle of guinea pig superfused with simulated ischemia (SI) solution (K+: 13 mM, pH: 6.0, pO2: 20-30 mmHg, glucose: 0 mM). After SI, both Vmax and conduction velocity decreased and r1 increased. When Vmax alone was taken into consideration, the measured conduction was slower than that predicted from the continuous cable theory. However, by compensating the value of Vmax by the change in r1, we could explain the change in measured conduction velocity by the cable theory. We conclude that, in myocardial ischemia, increase of r1 as well as diminished Vmax causes the conduction slowing and hence can lead to clinical arrhythmia such as reentrant tachycardia.