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[Correlation of limb and myocardial ischemia postconditioning with acute myocardial reperfusion injury].

Xinghua Zhang, Chunmei Li, Xiaojing Ma, Man Luo

Open publisher page 7 citations

Abstract

OBJECTIVE: We tested the hypothesis that remote postconditioning, which is induced by a single 5-min episode of femoral artery occlusion and reperfusion applied just before the onset of coronary artery reperfusion, protects the myocardium from reperfusion injury. METHODS: In anesthetized open-chest rabbits, the left anterior descending artery (LAD) was occluded for 30 min and reperfused for 3 hrs. All rabbits were randomly divided into four groups (n = 10 in each group): (1) CONTROL: LAD occlusion and reperfusion only, with no other intervention; (2) Myocardial ischemic preconditioning (Pre-con): Three cycles of myocardial ischemia (5 min) and reperfusion (5 min) preceded the index ischemia/reperfusion protocol; (3) Myocardial ischemic postconditionng (Post-con): After 30 min of LAD occlusion, reperfusion was initiated for 30 s followed by 30 s reocclusion. Three cycles of myocardial ischemia (30 s) and reperfusion (30 s) followed the index ischemia/reperfusion protocol. (4) Remote postconditioning (Re Post-con): After 24 min of LAD occlusion, the femoral artery was occluded for 5 min and released for 1 min before 3 hrs of LAD reperfusion. Myocardial infarct size and tissue myeloperoxidase (MPO) activity were determined at the end of the experiment. Plasma creatine kinase (CK) activity and malondialdehyde (MDA) activity were measured at baseline, the end of ischemia, and after 3 hrs of reperfusion respectively. RESULTS: Myocardial infarct size was significantly reduced in Pre-con (15.5% +/- 1.7%, P < 0.01), Post-con (16.15% +/- 2.05%, P < 0.01) and Re Post-con (17.11% +/- 1.70%, P < 0.01) groups as compared to CONTROL (31.46% +/- 1.28%). Results were confirmed by plasma CK activity (in Re Post-con 18.0 IU/g +/- 1.6 IU/g vs. CONTROL 45.6 IU/g +/- 5.5 IU/g). Plasma MDA was significantly less at 3 hrs of reperfusion in Pre-con (2.12 micromol/ml +/- 0.30 micromol/ml, P < 0.01), Post-con (2.17 micromol/ml +/- 0.24 micromol/ml, P < 0.01) and Re Post-con (2.16 micromol/ml +/- 0.33 micromol/ml, P < 0.01) than that in CONTROL (3.49 micromol/ml +/- 0.32 micromol/ml). Neutrophil accumulation (MPO activity) in the area at risk was less in Pre-con (1.43 U/100 g +/- 0.32 U/100 g, P < 0.01), Post-con (2.26 U/100 g +/- 0.28 U/100 g, P < 0.01) and Re Post-con (2.45 U/100 g +/- 0.28 U/100 g, P < 0.01) than that in CONTROL (5.44 U/100 g +/- 0.46 U/100 g). CONCLUSION: Remote limb postconditioing applied just before the onset of coronary artery reperfusion provides potent myocardial infarct size reduction, which is similar to the cardioprotective effect of myocardial postconditioning exerted during the first minutes of coronary reperfusion. The potential mechanism of this inter-organ remote postconditioning phenomenon might be associated with decreasing the injury caused by oxygen free radicals and strengthening the action of antioxidation.

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What this paper is about

OBJECTIVE: We tested the hypothesis that remote postconditioning, which is induced by a single 5-min episode of femoral artery occlusion and reperfusion applied just before the onset of coronary artery reperfusion, protects the myocardium from reperfusion injury. METHODS: In anesthetized open-chest rabbits, the left anterior descending artery (LAD) was occluded for 30 min and reperfused for 3 hrs. All rabbits were randomly divided into four groups (n = 10 in each group): (1) CONTROL: LAD occlusion and reperfusion only, with no other intervention; (2) Myocardial ischemic preconditioning (Pre-con): Three cycles of myocardial ischemia (5 min) and reperfusion (5 min) preceded the index ischemia/reperfusion protocol; (3) Myocardial ischemic postconditionng (Post-con): After 30 min of LAD occlusion, reperfusion was initiated for 30 s followed by 30 s reocclusion. Three cycles of myocardial ischemia (30 s) and reperfusion (30 s) followed the index ischemia/reperfusion protocol. (4) Remote postconditioning (Re Post-con): After 24 min of LAD occlusion, the femoral artery was occluded for 5 min and released for 1 min before 3 hrs of LAD reperfusion. Myocardial infarct size and tissue myeloperoxidase (MPO) activity were determined at the end of the experiment. Plasma creatine kinase (CK) activity and malondialdehyde (MDA) activity were measured at baseline, the end of ischemia, and after 3 hrs of reperfusion respectively. RESULTS: Myocardial infarct size was significantly reduced in Pre-con (15.5% +/- 1.7%, P < 0.01), Post-con (16.15% +/- 2.05%, P < 0.01) and Re Post-con (17.11% +/- 1.70%, P < 0.01) groups as compared to CONTROL (31.46% +/- 1.28%). Results were confirmed by plasma CK activity (in Re Post-con 18.0 IU/g +/- 1.6 IU/g vs. CONTROL 45.6 IU/g +/- 5.5 IU/g). Plasma MDA was significantly less at 3 hrs of reperfusion in Pre-con (2.12 micromol/ml +/- 0.30 micromol/ml, P < 0.01), Post-con (2.17 micromol/ml +/- 0.24 micromol/ml, P < 0.01) and Re Post-con (2.16 micromol/ml +/- 0.33 micromol/ml, P < 0.01) than that in CONTROL (3.49 micromol/ml +/- 0.32 micromol/ml). Neutrophil accumulation (MPO activity) in the area at risk was less in Pre-con (1.43 U/100 g +/- 0.32 U/100 g, P < 0.01), Post-con (2.26 U/100 g +/- 0.28 U/100 g, P < 0.01) and Re Post-con (2.45 U/100 g +/- 0.28 U/100 g, P < 0.01) than that in CONTROL (5.44 U/100 g +/- 0.46 U/100 g). CONCLUSION: Remote limb postconditioing applied just before the onset of coronary artery reperfusion provides potent myocardial infarct size reduction, which is similar to the cardioprotective effect of myocardial postconditioning exerted during the first minutes of coronary reperfusion. The potential mechanism of this inter-organ remote postconditioning phenomenon might be associated with decreasing the injury caused by oxygen free radicals and strengthening the action of antioxidation.

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Available abstract

OBJECTIVE: We tested the hypothesis that remote postconditioning, which is induced by a single 5-min episode of femoral artery occlusion and reperfusion applied just before the onset of coronary artery reperfusion, protects the myocardium from reperfusion injury. METHODS: In anesthetized open-chest rabbits, the left anterior descending artery (LAD) was occluded for 30 min and reperfused for 3 hrs. All rabbits were randomly divided into four groups (n = 10 in each group): (1) CONTROL: LAD occlusion and reperfusion only, with no other intervention; (2) Myocardial ischemic preconditioning (Pre-con): Three cycles of myocardial ischemia (5 min) and reperfusion (5 min) preceded the index ischemia/reperfusion protocol; (3) Myocardial ischemic postconditionng (Post-con): After 30 min of LAD occlusion, reperfusion was initiated for 30 s followed by 30 s reocclusion. Three cycles of myocardial ischemia (30 s) and reperfusion (30 s) followed the index ischemia/reperfusion protocol. (4) Remote postconditioning (Re Post-con): After 24 min of LAD occlusion, the femoral artery was occluded for 5 min and released for 1 min before 3 hrs of LAD reperfusion. Myocardial infarct size and tissue myeloperoxidase (MPO) activity were determined at the end of the experiment. Plasma creatine kinase (CK) activity and malondialdehyde (MDA) activity were measured at baseline, the end of ischemia, and after 3 hrs of reperfusion respectively. RESULTS: Myocardial infarct size was significantly reduced in Pre-con (15.5% +/- 1.7%, P < 0.01), Post-con (16.15% +/- 2.05%, P < 0.01) and Re Post-con (17.11% +/- 1.70%, P < 0.01) groups as compared to CONTROL (31.46% +/- 1.28%). Results were confirmed by plasma CK activity (in Re Post-con 18.0 IU/g +/- 1.6 IU/g vs. CONTROL 45.6 IU/g +/- 5.5 IU/g). Plasma MDA was significantly less at 3 hrs of reperfusion in Pre-con (2.12 micromol/ml +/- 0.30 micromol/ml, P < 0.01), Post-con (2.17 micromol/ml +/- 0.24 micromol/ml, P < 0.01) and Re Post-con (2.16 micromol/ml +/- 0.33 micromol/ml, P < 0.01) than that in CONTROL (3.49 micromol/ml +/- 0.32 micromol/ml). Neutrophil accumulation (MPO activity) in the area at risk was less in Pre-con (1.43 U/100 g +/- 0.32 U/100 g, P < 0.01), Post-con (2.26 U/100 g +/- 0.28 U/100 g, P < 0.01) and Re Post-con (2.45 U/100 g +/- 0.28 U/100 g, P < 0.01) than that in CONTROL (5.44 U/100 g +/- 0.46 U/100 g). CONCLUSION: Remote limb postconditioing applied just before the onset of coronary artery reperfusion provides potent myocardial infarct size reduction, which is similar to the cardioprotective effect of myocardial postconditioning exerted during the first minutes of coronary reperfusion. The potential mechanism of this inter-organ remote postconditioning phenomenon might be associated with decreasing the injury caused by oxygen free radicals and strengthening the action of antioxidation.

Key concepts: Medicine, Cardiology, Reperfusion injury, Ischemia, Internal medicine, Occlusion, Creatine kinase, Femoral artery

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[Correlation of limb and myocardial ischemia postconditioning with acute myocardial reperfusion injury]. — Research Paper | ScholarLens