| ForewordMyocardial ischemia-reperfusion(ischemic reperfusion,I/R) injury is a common clinical practice of organs and tissue injury,its precise mechanism is not yet very clear. The results show that myocardial ischemia-reperfusion injury is an acute inflammatory response,including ischemia-reperfusion activated JAKS-STATS systems,research has shown that,STAT-1 produced an increase is a result of cardiac dysfunction and myocardial cell necrosis of one of the important reasons At the same time,the expression of STAT-3 can significantly increase the reduction of myocardial cell injury and contribute to ischemia improves cardiac function,reduced infarct size and the number of apoptotic cells.In recent years,on the I/R injury mechanism of the increasing depth of understanding of the protection of immature myocardium to further deepen and put forward some new protection strategy.Of these,erythropoietin (erythropoietin) for myocardial protection attracted attention.EPO is a stimulation of bone marrow hematopoietic glycoprotein hormones, primarily in renal cortex and medulla at the junction of juxtaglomerular cell synthesis, molecular weight 30.4kd,a major role to promote elytroid progenitor cell differentiation into mature red blood cells and split,it has been widely for the treatment of renal failure,chemotherapy and surgery for various reasons,such as caused by anemia.As research has shown that EPO receptors(erythropoietin receptor,EPOR) widely exists in the cardiovascular system,in the cardiovascular system has a wide range of biology other than hematopoietic role,research has shown that,EPO through the surface of the target cell membrane and play a role combining EPOR of. Myocardial protection in various experimental studies can directly protect ventricular function,anti-endothelial apoptosis in myocardial cells,reducing the role of myocardial infarct size.In this study,the work of Langendorff isolated heart model,ruled out the neurohumoral and peripheral vascular resistance and other factors on the drug effects observed EPO injection on myocardial ischemia-reperfusion injury have protective effects,and to explore its possible mechanisms of the protective effect.Materials and Methods14～21d-born Japanese long ear rabbits 32(China Medical University animal hospital room Shengjing),weighing 210～300g,male and female informal.32 rabbits were randomly divided into 4 groups of 8.A group for the control group,B1,B2,B3 Group of EPO pretreatment group.Model set up at 24 hours before,EPO pretreatment group by intraperitoneal injection of different doses of EPO(Shen Yang Pharmaceutical Production Ltd.),B1 group 3000U/Kg,B2 group 5000U/Kg,B3 Group 7000U/Kg,the control group by intraperitoneal injection of normal saline.Experiments with intraperitoneal injection of 10%immature 10ml/Kg urethane anesthesia,by intraperitoneal injection of 500IU heparin anticoagulation.The middle thoracic chest incision and the heart quickly removed and immediately immersed in 4℃KH solution, after aortic cannulation was made after the connection langendorff isolated heart perfusion device to 37℃KH retrograde perfusion fluid,perfusion pressure constant as 60mmHg.After 15min perfusion of the natural balance,the control group and EPO group with 4℃St.ThomasⅡcardiologic for cardiologic.Four groups of heart by the low temperature(12±1)℃cardiologic after 30min to 37℃KH solution to the resumption of reperfusion after the jump 120min.After the end of the experiment immediately to retain part of the left ventricular myocardium Add 4%Para formaldehyde,the fixed one week after the block were made of wax;another part of the left ventricular myocardium from -70℃in refrigerator to preserve frozen.Ischemia, respectively,before measurement of ischemia-reperfusion 30min,ischemia-reperfusion 60min,ischemia-reperfusion of the coronary effluent 120min the amount of fluid(CF), and outflow of fluid to retain the de facto 2ml,the experiment at ambient temperature refrigerator to preserve,immediately after the end of the experiment with automatic detection of its biological and chemical detectors creating kinas(CK) and lactate dehydrogenises(LDH) levels;the end of the experiment will be all the paraffin-block sections,the application of immunohistochemical method to observe myocardial reperfusion 120min STAT-3 and Bcl-2 expression.SPSS13.0 statistical software used for data processing,measurement data to mean±standard deviation(s) that the comparison group using repeated measures analysis of variance of data,compared with 22 multiple comparisons t test,P＜0.05 for difference statistical significance.Results1.The coronary effluent flow rate changes:compared with the control group, EPO group after ischemia-reperfusion coronary flow was significantly increased outflow of fluid(P＜0.05),EPO pretreatment group 3 group,B2,B3 between the two groups no significant difference;but with the B1 group,B2,B3 were significantly lower,the difference was statistically significant.2.The coronary effluent fluid creatine kinase and lactate dehydrogenase changes: compared with the control group,EPO after ischemia-reperfusion group at each time point of creatine kinase and lactate dehydrogenase was significantly lower(P＜0.05). EPO pretreatment group 3 group,B2,B3 the difference between the two groups was not significant;However,compared with the B1 group,B2,B3 were significantly lower, the difference was statistically significant.3.Myocardial STAT-3 and Bcl-2 expression changes:A group without expression,EPO group after ischemia-reperfusion of the STAT-3 and Bcl-2 expression was significantly increased;EPO pretreatment group 3 group,B2,B3 obvious differences between the two groups;but B1 was significantly increased.Conclusion1.EPO pre-treatment can significantly reduce the myocardial ischemia-reperfusion injury of the immature myocardium has a role in myocardial protection.2.5000 U/kg,7000U/kg protective effect of preconditioning was no significant difference,but the difference between pre-treatment with 3000U/kg Obviously,there are statistically significant.3.EPO pretreatment significantly increased through the myocardial tissue of STAT-3 and Bcl-2 anti-apoptotic gene expression to achieve its myocardial protective effect of myocardial;... |
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