Experiments were performed to test the hypothesis that a reduction in the space constant contributes to slow conduction in the infarcted myocardium of dogs 5-8 days after coronary artery occlusion and reperfusion. Standard microelectrode techniques were used to measure action potential characteristics and conduction velocity parallel to fiber orientation in normal and infarcted ventricular epicardial strips superfused in a tissue bath. The space constants were determined by measuring the decay of the transmembrane steady state electrotonic potential with distance from a suction electrode current source. In eight normal epicardial preparations, conduction velocity ranged between 0.305 and 0.603 m/sec, and the space constant was between 0.712 and 1.202 mm. In 10 infarcted epicardial preparations, in regions of slow conduction (0.032-0.299 m/sec), the space constant was reduced to values between 0.281 and 0.917 mm. Action potential amplitude and maximum rate of depolarization were also reduced in infarcted myocardium. There was a direct relationship between conduction velocity and space constant and maximum rate of depolarization. In infarcted tissues, two types of slow conduction occurred. Slow conduction was uniform down to a velocity of approximately 0.181 m/sec, and a space constant of 0.523 mm. Below these values, conduction was discontinuous with prepotentials associated with the action potential upstroke. Indirect evidence from our studies suggests that a depression in action potential depolarization and an increase in effective axial resistance contribute approximately equally to uniform slow conduction in the infarcted myocardium.