The present study aimed to elucidate the mechanism of myocardial damage induced by simulated transport stress.Sprague Dawley rats were subjected to 35℃ and 60rpm (0.1 × g, rcf) on a constant temperature shaker.The blood samples was prepared for detection of epinephrine (E), norepinephrine (NE), and serum cardiac troponin T (Ctnt) ; myocardium samples was prepared for morphological examination and signaling protein quantitative.The result showed that plasma norepinephrine (NE) and epinephrine (E) concentrations increased in all stressed groups (P < 0.01).Levels of serum cardiac troponin T (Ctnt) were elevated in both the S2d (P < 0.05) and S3d groups (P <0.01).Morphological observation demonstrated obvious microstructure and ultrastructure damage after simulated transport stress.There was also a significant increase in the number of TUNEL-positive cardiomyocytes in stressed hearts.Western blot analysis found that the mitogen-activated protein kinase (MAPK) pathways were activated by strengthening phosphorylation of ASK—1 ,JNK,P38 and ERK in rat myocardial tissue after simulated transport stress (P < 0.05, P < 0.01).In addition, the ratio of pro-apoptotic Bax and anti-apoptotic Bcl—2 proleins was increased in stressed rats (P < 0.01), and the amount of cleaved-caspase3 increased in all stressed rats (P <0.01).The expression of cleaved-caspase9 protein was also elevated in S2d and S3d groups (P <0.01).Consequently simulated transport stress induced obvious myocardial damage,which may be attributed to the activation of caspase 9—mediated mitochondrial apoptotic pathway and MAPK pathways.