Electrogenic Na(+)-K+ pump in Purkinje myocytes isolated from control noninfarcted and infarcted hearts.

We combined a method of Na+ loading (zero K+ exposure) with voltage-clamp techniques to determine whether malfunctioning of the Na(+)-K+ pump underlies the abnormalities in the resting potential and the repolarization process observed in subendocardial Purkinje cells dispersed from the canine infarcted ventricle (IZPCs) 24 h after coronary artery occlusion. Stimulation of the transient outward current (ipump) was produced by a 3-min exposure to zero K+ and then reexposure to 4 mM K+ Tyrode solution. We compared the properties of ipump in IZPCs to ipump in Purkinje cells dispersed from fiber strands (SPCs) or from the subendocardium of the normal hearts (NZPCs). For the holding potentials (mean values: SPC, -33 +/- 7; NZPC, -33 +/- 5; and IZPC, -35 +/- 4 mV), the time constant (tau) of ipump in IZPCs (55 +/- 18 s) was not significantly different (P greater than 0.05) from tau in SPCs (55 +/- 10 s) or NZPCs (57 +/- 11 s). Peak ipump (Imax) and total charge transfer (Q) in IZPCs were not different from control. In SPCs and NZPCs, there was an increase in Imax and Q when zero K+ exposure was prolonged to 6-8 min, whereas in some IZPCs, the increase in Imax or Q was smaller. We conclude that the Na(+)-K+ pump current kinetics are not altered in IZPCs compared with control. Thus the persistent electrophysiological abnormalities in IZPCs that can still be observed after single cell isolation (Boyden, P. A., A. Albala, and K. Dresdner. Circ. Res. 65: 955-970, 1989) are not explained by an alteration in the function of the Na(+)-K+ pump.