In order to explore the reason why hypokalemia could increase the vulnerable window (VW) for unidirectional conduction block in Long QT Syndromes (LQTS), we observed the effect of hypokalemia on the spatial gradients of Na channel conductance (G(Na)) and gating factors by using the LR91 1-dimensional heterogeneous virtual cardiac ventricular tissue model quatitively. The computer simulation experiments were divided into two groups, namely control and LQTS groups. The action potential was elicited after the basic stimulus S1 (-70 microA/microF, 1.5 ms) was given 10 times with basic cycle length (BCL) 500, 1000 and 2000 ms. To test the VW in unit of time (VWtime), the S1-S2 programmed stimuli were used with shortening S1S2 interval at the decrement of 1 ms. At the same time, the spatial gradients of Na channel conductance (G(Na)) and gating factors, m, h, j, were investigated. The APD and ionic channel currents were also detected under the conditions of normal and lower concentration of K+ outside of cell. We found that hypokalemia, LQTS and slow pacing rate enhanced the spatial gradient of G(Na) by increasing the spatial gradient of inactive gating factors h x j. The results also showed that hypokalemia deduced the peak values of I(K) and I(K1), which prolonged the action potential duration and enlarged the repolarization dispersion in this 1-D tissue cable model. Possibly these are the important factors to cause the spatial gradient of h x j and G(Na). enlargement. These changes increase the incidence of unidirectional conduction block of VW, and are vital reasons to increase the possibility of ventricular arrhythmia generation.