In this paper, to analyze the functional influence of the early stage of global ischemia on cardiac electrical activity and subsequently on ventricular arrhythmia, we take into account of three main pathophysiological consequences of ischemia: hyperkalaemia, acidosis, and anoxia, and develop a human ventricular cell and tissue ischemic model that combines a detailed biophysical description of the excitation kinetics of human ventricular cells. Based on the model, the APDR curves, ERPR curves, vulnerable window, and CVR curves under control and ischemic condition are computed separately. The experimental results show that global ischemia can reduce APD, and slow down CV. Meanwhile since global ischemia decreases slope of APDR and increases ERP, the induced re-entry can be maintained stably which is not prone to degenerate into ventricular fibrillation. And due to a comparatively longer ectopic stimulation length to ensure the formation of reentry, global ischemia decreases the probability to arrhythmia in some extent although the increased tissue vulnerability.