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 m...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 pg/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-a （TNF-a） 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.展开更多
基金Project (No. 03III02) supported by the Capital Medical Development Research Fund of China
文摘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 pg/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-a （TNF-a） 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.
