摘要
BACKGROUND: Rapid and complete reperfusion has been widely adopted in the treatment of patients with acute myocardial infarction(AMI), but this process sometimes can cause severe reperfusion injury. This study aimed to investigate different patterns of post-conditioning in acute myocardial ischemia-reperfusion injury, and to detect the role of mitogen activated protein kinase(MAPK) during the injury.METHODS: Rats were randomly divided into five groups: sham group, reperfusion injury(R/I) group, gradually decreased reperfusion group(GDR group, 30/10-25/15-15/25-10/30 seconds of reperfusion/ischemia), equal reperfusion group(ER group, 20/20 seconds reperfusion/ischemia, 4 cycles), and gradually increased reperfusion group(GIR group, 10/30-15/25-25/15-30/10 seconds of reperfusion/ischemia). Acute myocardial infarction and ischemic post-conditioning models were established in the rats. Six hours after reperfusion, 3 rats from each group were sacrificed and myocardial tissues were taken to measure the expressions of phosphorylation of extracellular signalregulated protein kinase(P-ERK), phosphorylated c-Jun N-terminal kinase(P-JNK), mitogen-activated protein kinase p38(p38 MAPK), tumor necrosis factor-α(TNF-α), caspases-8 in the myocardial tissue, and cytochrome c in the cytosol using Western blot. Hemodynamics was measured at 24 hours after reperfusion, the blood was drawn for the determination of cardiac enzymes, and the heart tissue was collected for the measurement of apoptosis using TUNEL. One-way analysis of variance and the Q test were employed to determine differences in individual variables between the 5 groups.RESULTS: Three post-conditioning patterns were found to provide cardioprotection(P<0.05) compared with R/I without postconditioning. GIR provided the best cardioprotection effect, followed by ER and then GDR. Apoptotic index and serum marker levels were reduced more signifi cantly in GIR than in ER(P<0.05). The enhanced cardioprotection provided by GIR was accompanied with significantly increased lev
BACKGROUND： Rapid and complete reperfusion has been widely adopted in the treatment of patients with acute myocardial infarction （AMI）, but this process sometimes can cause severe reperfusion injury. This study aimed to investigate different patterns of post-conditioning in acute myocardial ischemia-reperfusion injury, and to detect the role of mitogen activated protein kinase （MAPK） during the injury. METHODS： Rats were randomly divided into five groups： sham group, reperfusion injury （R/ I） group, gradually decreased reperfusion group （GDR group, 30/10-25/15-15/25-10/30 seconds of reperfusion/ischemia）, equal reperfusion group （ER group, 20/20 seconds reperfusion/ischemia, 4 cycles）, and gradually increased reperfusion group （GIR group, 10/30-15/25-25/15-30/10 seconds of reperfusion/ischemia）. Acute myocardial infarction and ischemic post-conditioning models were established in the rats. Six hours after reperfusion, 3 rats from each group were sacrificed and myocardial tissues were taken to measure the expressions of phosphorylation of extracellular signal- regulated protein kinase （P-ERK）, phosphorylated c-Jun N-terminal kinase （P-JNK）, mitogen-activated protein kinase p38 （p38 MAPK）, tumor necrosis factor-a （TNF-a）, caspases-8 in the myocardial tissue, and cytochrome c in the cytosol using Western blot. Hemodynamics was measured at 24 hours after reperfusion, the blood was drawn for the determination of cardiac enzymes, and the heart tissue was collected for the measurement of apoptosis using TUNEL. One-way analysis of variance and the Q test were employed to determine differences in individual variables between the 5 groups. RESULTS： Three post-conditioning patterns were found to provide cardioprotection （P〈0.05） compared with R/I without postconditioning. GIR provided the best cardioprotection effect, followed by ER and then GDR. Apoptotic index and serum marker levels were reduced more significantly in GIR than in ER （P〈0.05）. The enhanced cardi
基金
supported by grants from the National Science Foundation of China(30740080)
Dean fund of the General Hospital of Jinan Military Command(2011Q08)
