Abstract: Objective: to investigate the inhibitory effects of a new mitogen activated protein kinase （MAPK） blocker PD098059 on the Angiotensin II （AngII） induced increase of cardiac myocyte viability, in order to observe whether the intracellular signal blocker can effectively interfere with the cellular energy metabolism and provide the new experimental evidence for the application of those agents in pharmacological therapy of congestive heart failure.Methods: Based on that the mitochondria of viable cells can act on MTT to produce formazan with light purple, we investigate the effect of AngII on the cultured myocyte viability and the intervention of PD098059 by means of colorimetric method.Results: Our results showed that AngII caused the gradual increase of formazan optical density （OD） in 12 hours, and the formazan OD reached the peak at 12 hour, thereafter decreased, even lower than the normal at 24 hour PD098059 did successfully and significantly antagonized the effect of AngII on the cardiac myocyte viability （P＜0 05 PD098059 group vs AngII group）.Conclusion: PD098059 could effectively antagonize the action of AngII on the cardiac myocyte viability It has important meanings for the application of intracellular signal blocker in pharmacological therapy of congestive heart failure in the future