Objective:To evaluate whether liposomal prostaglandin E1 (lipo-PGE1) can decrease reperfusion no-reflow in a catheter-based porcine model of acute myocardial infarction (AMI).Methods:Twenty-two male Chinese mini-swines were randomized into three groups:six in a sham-operation group,and eight each in the control and lipo-PGE1 groups.The distal part of the left anterior descending coronary artery (LAD) in the latter two groups was completely occluded for 2 h,and then reperfused for 3 h.Lipo-PGE1 (1 μg/kg) was injected 10 min before LAD occlusion until reperfusion for 1 h in the lipo-PGE1 group.Hemodynamic data and proinflammatory cytokines were examined before AMI,2 h after occlusion,and 1,2,and 3 h after reperfusion.Myocardial contrast echocardiography (MCE) and double staining were performed to evaluate the myocardial no-reflow area (NRA).Results:Left ventricular systolic pressure and end-diastolic pressure significantly improved in the lipo-PGE1 group after reperfusion compared with the control group and also 2 h after AMI (P<0.05 for both).MCE and double staining both showed that lipo-PGE1 decreased reperfusion NRA after AMI (P<0.05,P<0.01).Lipo-PGE1 decreased serum interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) after myocardial infarction reperfusion (P<0.05 for both).Conclusions:Lipo-PGE1 is cardioprotective in our porcine model of myocardial infarction reperfusion no-reflow,decreasing NRA and attenuating the inflammatory response. Objective: To evaluate whether liposomal prostaglandin E1 (lipo-PGE1) can decrease reperfusion no-reflow in a catheter-based porcine model of acute myocardial infarction (AMI). Methods: Twenty-two male Chinese mini-swines were randomized into three groups: six in a sham-operation group, and eight each in the control and lipo-PGE1 groups. distal part of the left anterior descending coronary artery (LAD) in the latter two groups were completely occluded for 2 h, and then reperfused for 3 Lipo-PGE1 (1 μg / kg) was injected 10 min before LAD occlusion until reperfusion for 1 h in the lipo-PGE1 group. Hemodynamic data and proinflammatory cytokines were examined before AMI, 2 h after occlusion, and 1,2, Results: Left ventricular systolic pressure and end-diastolic pressure significantly improved in the lipo-PGE1 group after reperfusion (MCE) and double staining were performed to evaluate the myocardial no-reflow area compared with the control group and also 2 h after AMI (P <0.05 for both) .MCE and double-staining both showed that lipo-PGE1 decreased reperfusion NRA after AMI (P <0.05, P <0.01) .Lipo-PGE1 decreased serum interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) after myocardial infarction reperfusion (P <0.05 for both). Conclusions: Lipo-PGE1 is cardioprotective in our porcine model of myocardial infarction reperfusion no-reflow, attenuating the inflammatory response.