AIM: To investigate the relationship between polyamine metabolism and hypoxia / ischemia( H / I)-induced cell apoptosis and to determine the mechanisms by which exogenous spermine protects cell apoptosis against AMI in rats. METHOD: The left anterior descending coronary artery( LAD) of the Wistar rats were ligated,and neonatal rat cardiomyocytes were placed under hypoxic conditions for 24 h to establish the model of AMI( or H / I). Exogenous spermine was administered by intraperitoneal injection(2. 5 mg / kg daily for 7 days) in vitro and subjected to the cell medium at 5 μmol / L as a pre-treatment therapy. RESULTS: AMI( or H / I) induced an increase in polyamine catabolized enzyme SSAT and a decrease in polyamine biosynthesis enzyme ODC,which result in endogenous spermine and spermidine decrease and putrescine increase. At the same time,AMI( or H / I) lowered cardiac function,increased c Tn I and CK-MB concentrations,aggravated myocardial infarct size,cardiomyocyte damage and apoptosis,raised ROS generation,increased the expression of cleaved caspase-3,cleaved caspase-9 and endoplasmic reticulum stress( ERS)-related proteins,promoted the release of cytochrome C and m PTP opening,down-regulated Bcl-2 expression and the phosphorylation of ERK1 /2,PI3 K,Akt and GSK-3β,and activated PERK and e IF2α phosphorylation. Spermine pre-treatment reversed the above-motioned changes. CONCLUSION: AMI(or H/I) could induce cardiomyocyte apoptosis and polyamine metabolism disorder. Exogenous spermine attenuates cardiac injury through scavenging the ROS and inhibiting m PTP opening and ERS injury. These findings provide a novel target for the prevention of apoptosis in the setting of AMI. AIM: To investigate the relationship between polyamine metabolism and hypoxia / ischemia (H / I) -induced cell apoptosis and to determine the mechanisms by which exogenous spermine protects cell apoptosis against AMI in rats. METHODS: The left anterior descending coronary artery (LAD) of the Wistar rats were ligated, and neonatal rat cardiomyocytes were placed under hypoxic conditions for 24 h to establish the model of AMI (or H / I). Exogenous spermine was administered by intraperitoneal injection (2.5 mg / kg daily for 7 days ) in vitro and subjected to the cell medium at 5 μmol / L as a pre-treatment therapy. RESULTS: AMI (or H / I) induced an increase in polyamine catabolized enzyme SSAT and a decrease in polyamine biosynthesis enzyme ODC, which results in At the same time, AMI (or H / I) lowered cardiac function, increased c Tn I and CK-MB concentrations, aggravated myocardial infarct size, cardiomyocyte damage and apopto sis, raised the expression of cleaved caspase-3, cleaved caspase-9 and endoplasmic reticulum stress (ERS) -related proteins, promoted the release of cytochrome C and m PTP opening, down-regulated Bcl-2 expression and the phosphorylation of ERK1 / 2, PI3 K, Akt and GSK-3β, and activated PERK and e IF2α phosphorylation. Spermine pre -diacted above-motioned changes. CONCLUSION: AMI (or H / I) could induce cardiomyocyte apoptosis and polyamine metabolism disorder. Exogenous spermine attenuates cardiac injury through scavenging the ROS and inhibiting m PTP opening and ERS injury. These findings provide a novel target for the prevention of apoptosis in the setting of AMI.